Biomedical subjects

L J Pelliniemi

Publications and source records attributed to L J Pelliniemi.

At least 19 recordsLinked to original sources

PubMed2001

Structural and regulatory macromolecules in sex differentiation of gonads.

The manifestations of sex determination were studied in vivo by detection and localization of structural and regulatory macromolecules (type IV collagen alpha 1, alpha 2, alpha 3, alpha 4, and alpha 5; laminin alpha 5, beta 1, and beta 2; cytokeratins 18 and 19, desmin, vimentin; integrin alpha(6;) anti-Müllerian hormone (AMH); and SOX9 in developing male and female gonads by light and electron microscopy, immunocytochemistry, and protein analysis. The goal has been to find sex-related differences and on this basis to offer new molecules to be tested further for a possible role in sex determination. Specific antibodies for each molecule or for a defined subchain were used to allow tentative correlation with specific genes. Sex-dependent differences in timing and localization were found in laminin alpha 5; collagen, alpha 3, alpha 4, and alpha 5; cytokeratin 19; AMH; and SOX9. On this basis we hypothesize that the transcription factors for the mentioned structural proteins must be directly or indirectly involved in the regulatory chain of gonadal sex differentiation. Especially promising is the finding in the rat that laminin alpha 5 chain disappears from the basement membrane of embryonic testicular cords (Sertoli cells) when AMH secretion by Sertoli cells starts, and that the same chain reappears as the AMH disappears two weeks after birth. Via AMH as an intermediary factor, we now have for the first time a putative cascade of regulatory molecules from SRY, SF1, and SOX9 to a component of a structural protein (laminin alpha 5 chain) which directly participates in the formation of the basement membrane of the testicular cords. J. Exp. Zool. 290:523-528, 2001.

Animals↗

PubMed2001

Age-dependent changes in the expression of matrix components in the mouse eye.

Although the presence of 'cartilage-specific' collagens in the eye has been documented earlier, very little is known about their synthesis rates during ocular development, growth and aging. The purpose of the present study was to follow changes in the mRNA levels and distribution of key components of the extracellular matrix in the eyes of normal and transgenic Del1 mice, harboring a short deletion mutation in the type II collagen gene, during ocular growth and aging. Total RNAs extracted from mouse eyes were studied by Northern analysis for mRNA levels of type I, II, III, VI, IX and XI collagens, biglycan, fibromodulin and decorin. A predominant finding of the present study was the marked reduction in the mRNA levels of type I and II collagens in the eye upon aging. The changes in the mRNA levels of type III and VI collagen and proteoglycans were smaller. Localization of type II and IX collagen in the eye was performed by immunohistochemistry. Despite the reduction in the type II collagen mRNA levels, immunohistochemistry confirmed widespread distribution of the protein also in aging mouse eyes, suggesting its slow turnover. Although the Del1 mutation caused gradual degenerative lesions in the eyes, the distribution of the protein remained essentially unchanged. The widespread distribution and marked downregulation of type II collagen production in the mouse eye upon aging probably explain the gradual development of degenerative lesions, particularly in the eyes of transgenic Del1 mice, where production of mutant type II collagen chains also contributes to the process.

Aging↗

PubMed2001

Heat shock proteins, HSP25 and HSP70, and apoptosis in developing endocardial cushion of the mouse heart.

Formation of the atrioventricular channels and valves from the endocardial cushion occurs through growth and remodeling of the initial endocardial cushion. This process requires balanced coordination of proliferation and apoptosis by still unknown factors. To detect a possible role for the heat shock proteins 25 and 70 (HSP25 and HSP70) as apoptosis-associated proteins and differentiation factors in the development of the endocardial cushion, we analyzed their temporal and regional occurrence during cell proliferation and apoptosis in E11-E17 embryos. The distribution and timing of these events and factors were consistent with the hypothesis that HSP25 is related to myocardial development whereas HSP70 is related to differentiation of the endocardial cushion by cell proliferation and apoptosis.

Animals↗

PubMed2001

Overlapping and differential localization of Bmp-2, Bmp-4, Msx-2 and apoptosis in the endocardial cushion and adjacent tissues of the developing mouse heart.

The bone morphogenetic proteins BMP-2 and BMP-4 and the homeobox gene MSX-2 are required for normal development of many embryonic tissues. To elucidate their possible roles during the remodeling of the tubular heart into a fully septated four-chambered heart, we have localized the mRNA of Bmp-2, Bmp-4, Msx-2 and apoptotic cells in the developing mouse heart from embryonic day (E)11 to E17. mRNA was localized by in situ hybridization, and apoptotic cells by TUNEL (TDT-mediated dUTP-biotin nick end-labeling) as well as by transmission electron microscopy. By analyzing adjacent serial sections, we demonstrated that the expression of Msx-2 and Bmp-2 strikingly overlapped in the atrioventricular canal myocardium, in the atrioventricular junctional myocardium, and in the maturing myocardium of the atrioventricular valves. Bmp-4 was expressed in the outflow tract myocardium and in the endocardial cushion of the outflow tract ridges from E12 to E14. Msx-2 appeared in the mesenchyme of the atrioventricular endocardial cushion from E11 to E14, while Bmp-2 and Bmp-4 were detected between E11 and E14. Apoptotic cells were also detected in the mesenchyme of the endocardial cushion between E12 and E14. Our results suggest that BMP-2 and MSX-2 are tightly linked to the formation of the atrioventricular junction and valves and that BMP-4 is involved in the development of the outflow tract myocardium and of the endocardial cushion. In addition, BMP-2, BMP-4 and MSX-2 and apoptosis seem to be associated with differentiation of the endocardial cushion.

Animals↗

PubMed2001

Management of testicular cancer--16 years' experience from southwest Finland.

OBJECTIVE: This study investigated the outcome of testicular cancer treatment in Finland. MATERIAL AND METHODS: Data on 88 testicular cancer patients treated in Turku University Central Hospital between 1976 and 1992 were studied to analyse outcome and survival. RESULTS: The histological diagnosis was seminoma for 39 patients and non-seminoma for 49 patients. Two seminoma patients relapsed (5%) and one patient died of progressive disease (3%; initially stage II seminoma). Eleven non-seminoma patients relapsed (22%), nine of whom were cured with chemotherapy. Four non-seminoma patients died of progressive disease (8%; initially one stage I non-seminoma and three stage III non-seminomas). The median time to relapse after the completion of treatment was 9 months (range 3-50 months). Non-seminoma patients had significantly more relapses than seminoma patients (p = 0.03). Most relapses (73% of the non-seminoma relapses) were found among the stage I non-seminoma patients who had not received adjuvant chemotherapy, while none of the stage I seminoma patients relapsed (p = 0.007). CONCLUSIONS: Close surveillance is important for all non-seminoma patients to guarantee the early detection and treatment of recurrent disease. Treatment and surveillance should be covered by national guidelines and be conducted in centres with special interest in this rare but mostly curable cancer.

Adolescent↗

PubMed2001

Identification of alpha6beta1 integrin positive cells in synovial lining layer as type B synoviocytes.

OBJECTIVE: In rheumatoid arthritis (RA) the synovial lining is responsible for cartilage destruction. Laminin is one of the major matrix molecules surrounding the lining cells. We investigated the laminin adhesion mechanism of synovial lining cells by analyzing the presence of its receptor, alpha6beta1 integrin, on type A and type B synoviocytes. METHODS: The alpha6 integrin subunit and a macrophage marker were simultaneously localized by immunohistochemistry in 29 RA derived, 6 osteoarthritis derived, and 2 healthy synovial samples by light and electron microscopy. We also used enzyme treatments to release cells from synovial tissue samples and localized the same antigens on adherent cells. RESULTS: The alpha6beta1 integrin positive cells were localized in basal areas of the lining layer and many of them were negative for the macrophage markers. By immunolabeling electron microscopy the alpha6 integrin positive cells were confirmed to represent the fibroblast-like type B cells. Further, in freshly isolated synoviocyte cultures the type B cells were positive for alpha6 integrin, whereas all other cell types were negative for this laminin receptor. CONCLUSION: Integrin alpha6beta1 is known to be a laminin receptor of endothelial cells, adipocytes, and macrophages, not usually expressed on fibroblasts. However, in synovial lining layer it is expressed on fibroblastic type B cells, but the macrophage population is negative. The unique characteristics of synovial lining cells distinguish them from other connective tissue cells and must be taken into account in all considerations of the pathogenic mechanisms of rheumatoid disease.

Arthritis, Rheumatoid↗

PubMed2000

Sox9 protein in rat sertoli cells is age and stage dependent.

We studied the location of Sox9 protein in the embryonic, juvenile, and adult rat testis by immunohistochemistry and immunoblotting. Sox9 belongs to a family of Sox proteins that are transcription factors and important in several developmental processes. In the incipient embryonic testis, Sox9 was prominently present in the gonadal blastema. With further embryonic differentiation, Sox9-positive cells arranged in the periphery of the testicular cords, showing the location of the Sertoli cells. Thereafter the immunoreaction for Sox9 gradually declined and was only weakly detectable in the 2-day-old postnatal rat testis. This situation remained for some period of time. In the 15-day-old rat testis, Sox9 protein strongly reappeared in the testicular cords. In the adult, the Sertoli cells of most regions of the seminiferous tubules were positive for Sox9. The strongest reaction for Sox9 was found in the dark zone. However, clearly negative or only weakly positive spermatogenic stages for the protein were also found, as seen for example in the pale zone. In fertile 1-year-old rats this basic situation was still detectable. Analyzed rat ovaries were all negative for Sox9, showing the sex-specific nature of Sox9. The results showed that Sox9 protein is distinctly present in the developing and mature Sertoli cells, but that its presence and amount is dependent on the age and the spermatogenetic stage within the seminiferous tubuli. The prominent presence of Sox9 in the incipient testis and at puberty suggests that this protein is needed at important phases of aggregation and reorganization of the Sertoli cells. The age and stage-specific presence of Sox9 in the testicular cords and in the seminiferous tubules of the adult suggests that Sox9 also may have a pivotal role in germ cell differentiation.

Aging↗

PubMed2000

Effect of etoposide on experimental testicular teratoma in 129/SvJ mice.

To study the effects of etoposide on experimental testicular teratoma in 129/SvJ mouse we analysed the tumour growth, differentiation, apoptosis and the localisation of mdr1 P-glycoprotein (mdr1-Pgp). In this model the implanted gonadal ridges developed into testicular teratomas in 17 out of 56 implanted testes (30%) and in 14 out of 28 mice (50%). The tumour-bearing mice were treated with etoposide on 4 successive days either 4 weeks or 6 weeks after implantation, and killed 7 days after the last dose. The mice in the control groups did not receive etoposide. The teratomas consisted mainly of neural tissue. The etoposide-treated 4-week teratomas, but not the 6-week teratomas, were significantly smaller than those in the corresponding control groups. The density of apoptotic cells and the distribution of the mdr1-Pgp were not altered by etoposide. The decreased proportion of immature neuroectodermal tissue components was observed in all treated teratomas, converting the histology towards that of a mature teratoma. In addition, a low proportion of immature tissue components was frequently combined with a low density of apoptotic cells. In conclusion, etoposide decreased the immature tissue components of teratomas, while mature tissues remained unaffected. These results may have clinical relevance in man, since they confirm that postchemotherapy mature teratomas cannot be treated with chemotherapy. Despite benign histology, the human residual tumours have a significant malignant potential and require complete surgical excision and close surveillance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1999

Apoptosis in the pattern formation of the ventricular wall during mouse heart organogenesis.

Apoptosis is an important mechanism in organogenesis, but its role in heart development has been poorly characterized. We have here studied apoptosis in the developing ventricular wall of mouse embryonic heart. Developing mice hearts on days 11 to 16 of gestation were studied using in situ end-labeling of degraded DNA (TUNEL), immunocytochemistry of regulatory genes Bcl-2 and Bax, and light and electron microscopy. TUNEL end-labeled apoptotic cells were found in the ventricular wall on days 11 to 16 of gestation. The proportions of apoptotic cells of all cells in the ventricular wall differed between the trabecular and compact regions (P = 0.003) and between the days of gestation (P = 0.0001), the calculated apoptotic index was greater in the compact region at all ages except day 14. Ultrastructural analysis showed typical apoptotic shrinkage, chromatin degradation, and apoptotic bodies in several myoblastic and myocardial endothelial cells which were also positive by DNA end-labeling. Immunocytochemical reaction for the apoptosis checkpoint proteins in the ventricular wall showed clearly more Bcl-2 positive cells than Bax positive cells. The numerical densities of all cells in the compact and trabecular regions remained always higher in the compact region (P = 0.04) despite the fact that apoptosis was present in both areas at the same time. In conclusion, apoptosis takes place in the developing myocardial muscle as well as the myocardial endothelium during ventricular morphogenesis on days 11 through 16 and decreases clearly on day 16. We suggest that apoptosis and its regulatory factors are closely involved in the morphogenesis of the ventricular wall of the mammalian heart.

Animals↗

PubMed1999

Presence of anti-Müllerian hormone correlates with absence of laminin alpha5 chain in differentiating rat testis and ovary.

The distribution of anti-Müllerian hormone (AMH) and laminin (Ln) alpha5 chain in differentiating rat testis and ovary were studied by immunohistochemistry. In the incipient embryonic male gonad a weak reaction for Ln alpha5 chain, but not for AMH, was detected. With further prenatal development, Ln alpha5 chain rapidly disappeared from the basement membrane (BM) of the incipient testicular cords in parallel with the appearance of AMH in the Sertoli cells. After birth, Ln alpha5 chain reappeared in the BMs of the cords with the decline and disappearance of AMH from the respective Sertoli cells. In the corresponding stages of the ovary, Ln alpha5 chain was present in the BM of the prenatal gonadal cords and in postnatal primordial follicles. The cells of those epithelia were negative for AMH. With the growth of the follicles, Ln alpha5 chain disappeared from the BM when AMH appeared in the epithelial follicular cells. The present results show that male and female gonadal epithelia negative for Ln alpha5 chain were positive for AMH, and that epithelia positive for Ln alpha5 chain were negative for AMH. Thus, epithelial Ln alpha5 chain and AMH as a product of the same cell seemed to exclude each other. The results require an explanation why Ln alpha5 chain has to be excluded from the BM of the epithelia during the secretion of AMH chain through the basal cell membrane to the surrounding tissues where it executes its important biological functions. These observations suggest a hypothesis that the production of both components is regulated by the same gene and factor system.

Animals↗

PubMed1999

Human vascular adhesion protein-1 in smooth muscle cells.

Human vascular adhesion protein-1 (VAP-1) is a dual-function molecule with adhesive and enzymatic properties. In addition to synthesis in endothelial cells, where it mediates lymphocyte binding, VAP-1 is expressed in smooth muscle cells. Here we studied the expression, biochemical structure, and function of VAP-1 in muscle cells and compared it to those in endothelial cells. VAP-1 is expressed on the plasma membrane of all types of smooth muscle cells, but it is completely absent from cardiac and skeletal muscle cells. In tumors, VAP-1 is retained on all leiomyoma cells, whereas it is lost in half of leiomyosarcoma samples. In smooth muscle VAP-1 predominantly exists as a approximately 165-kd homodimeric glycoprotein, but a trimeric (approximately 250 kd) form of VAP-1 is also found. It contains N-linked oligosaccharide side chains and abundant sialic acid decorations. In comparison, in endothelial cells dimeric VAP-1 is larger, no trimeric forms are found, and VAP-1 does not have N-glycanase-sensitive oligosaccharides. Unlike endothelial VAP-1, VAP-1 localized on smooth muscle cells does not support binding of lymphocytes. Instead, it deaminates exogenous and endogenous primary amines. In conclusion, VAP-1 in smooth muscle cells is structurally and functionally distinct from VAP-1 present on endothelial cells.

Amine Oxidase (Copper-Containing)↗

PubMed1999

Experimental testicular teratoma promotes formation of humoral immune responses in the host testis.

The testis is an immunologically privileged site. Very little is known about the factors regulating formation of immune responses elicited by a neoplasm in the testis. We have studied the immune response of the host testis against experimental testicular teratoma in mouse by localizing adhesion molecules (CD106, CD54, CD49d/CD29, CD44, CD18, CD8 and CD4), cytokines (IL-2, IL-4, IL-6, IL-10 and IL-12), T-cell costimulators (CD80, CD86) and the lipid antigen presenting molecule CD1d in the testis of 129/SvJ mice with and without experimental testicular teratoma. The testicular teratomas were induced by grafting male gonadal ridges from 12-day-old 129/SvJ mouse fetuses into testes of adult mice from the same strain. The tumors cultured intratesticularly for 2, 3, 4 and 8 weeks (three animals per time point) were used for immunocytochemistry. CD1d was detected in Sertoli cells and in some degenerated tubules of the host testis surrounding the graft. In the tumor, CD1d was detected in glandular epithelia, smooth muscle and in thin fibers of neural origin. IL-2 was observed in some blood vessels of the host testis and of the tumor and in occasional cell infiltrates around these vessels. Some tubular structures of the tumor were also positive for IL-2. IL-6 was detected in Sertoli cells of the normal testis and in Sertoli cells and in solitaryinterstitial cells as well as in the walls of some blood vessels of the host testis. The reaction for IL-6 was more prominent in the tubules apparently damaged by the growing tumor. In the tumor IL-6 was detected in epithelial structures, muscle cells, in thin fibers of neural origin and in some blood vessels. IL-10 was detected in individual cells in the interstitium and in degenerating tubules of the host testis. In the tumor the epithelial structures were positive for IL-10. The interstitium of the host testis was positive for CD106 and the embryonic testicular cords in the graft were also positive, but the tumor was negative. CD44 and CD18 were observed in some blood vessels and in degenerated tubules of the host testis. In the tumor CD44 and CD18 were occasionally observed in cartilage and in epithelial structures. The results of the present study suggest that cytokine microenvironment in the testis containing neoplastic tissue promotes activation of humoral immune responses. In addition, as the damaged seminiferous tubules expressed increased amounts of two cytokines promoting humoral immune responses, IL-6 and IL-10, it is possible that also in other conditions with damage to the tubules, humoral immune responses predominate.

Animals↗

PubMed1999

Characterization of the model for experimental testicular teratoma in 129/SvJ-mice.

An animal model of experimental testicular teratoma has been established to study how a teratoma affects the host testis and how the host testis reacts against the teratoma. 129/SvJ-mice were used as experimental animals. To induce the experimental testicular teratoma, male gonadal ridges from 12-day-old 129/SvJ-mouse fetuses were grafted into the testes of adult mice for 1-12 weeks. The developing tumour was analysed by light and electron microscopy and by immunocytochemical localization of transcription factors SOX9 and c-kit, glial fibrillary acidic protein (GFAP) and type IV collagen. Testicular teratoma was observed in 36 out of 124 testes with implanted fetal gonadal ridges (frequency 29%). One spontaneous testicular teratoma was observed in this material from 70 male mice (1.5%). One week after implantation intracordal clusters of cells were seen in embryonic testicular cords of the graft as the first sign of testicular teratomas. Four weeks after implantation the embryonic testicular cords had totally disappeared from grafts with teratomas, and the tumour tissue had enlarged the testis and invaded the interstitium of the host testis. It consisted of solitary pieces of immature cartilage as well as of glial cells and of primitive neuroepithelium. Six to eight weeks after implantation the tumour tissue had expanded so that the enlarged testis could be detected by macroscopic enlargement of the scrotum. The testicular tissue of the host had practically disappeared, and only solitary disrupted seminiferous tubules of the host were seen surrounding the teratoma. Neuroepithelial structures of some teratomas cultured for 8 weeks had cells with a granular nucleus as a sign of obvious apoptosis. Eleven to 12 weeks after implantation the growth of the teratoma had stopped, and the histology corresponded to that of a mature cystic teratoma. GFAP, SOX9 and type IV collagen were strongly positive in some parts of the tumours cultured for 4 and 8 weeks, while only occasional c-kit-positive areas were observed in tumours cultured for 8 weeks. As conclusions: (1) the metastasizing capacity of the experimental testicular teratoma is very low during 12 weeks, but the behaviour of the tumour in the testicular tissue of the graft is invasive; (2) the growth of experimental testicular teratomas cease 6-8 weeks after implantation of the fetal gonadal ridges with the obvious apoptosis of the immature tissue components; (3) the model of experimental testicular teratoma in the mouse is suitable for studying how the teratoma affects the host testis and how the host testis reacts to teratoma.

Animals↗

PubMed1999

Sex-specific localization of laminin alpha 5 chain in the differentiating rat testis and ovary.

The localization of laminin (Ln) alpha 5, beta 1 and beta 2 chains in the differentiating rat testis and ovary was studied by immunolabeling light and electron microscopy. The initial formation of the male and female gonadal blastemas included an emergence of Ln alpha 5 and beta 1 chains, but not of Ln beta 2 chain. The sexual differentiation of the embryonic male gonadal cords included rapid sex-specific disappearance of the incipient Ln alpha 5 chain. The rete testis cords, in contrast, remained positive for Ln alpha 5 chain. In the postnatal testis, the Ln alpha 5 chain reappeared in Ln beta 1 chain-positive cord basement membranes, which also became positive for Ln beta 2 chain. The differentiating myoid cells also gradually became positive for both Ln alpha 5 and Ln beta 1 chains. In the ovary Ln alpha 5 chain persisted in BMs of the cords throughout the fetal phase. Small and newly formed follicles in the early postnatal rat ovary were also positive for Ln alpha 5 chain, whereas growing and large follicles were negative. During the early postnatal phase, Ln beta 1-chain positive follicular BMs became also positive for the Ln beta 2 chain. Basement membranes of testicular and ovarian surface epithelia contained the Ln alpha 5 chain throughout the study. The blood vessels of the male and female gonad showed differentiation-dependent variation in their reactivity for the Ln alpha 5 and beta 2 chains. The present results show that the Ln alpha 5 chain is an early molecular marker for sexual differentiation, which therefore may be regulated by the testis-determining factors. The results also show that in the early postnatal rat ovary, the follicular basement membranes are heterogeneous in their Ln content, which may offer a means to distinguish different follicular populations from each other and to identify the different stages of follicular growth.

Animals↗

PubMed1998

The polysialic acid units of the neural cell adhesion molecule N-CAM form filament bundle networks.

Polysialic acid is a developmentally regulated component in the neural cell adhesion molecule N-CAM which also occurs as the capsular polysaccharide of bacteria causing meningitis. Polysialic acid has been considered as a repulsive element that regulates intermolecular and intercellular adhesion. Using atomic force microscopy we unexpectedly find that oligomers of polysialic acid assemble with each other into filament bundle networks. Filaments were formed from oligomers containing 12 or more N-acetylneuraminic acid residues, and they were sensitive to sialidase digestion. The networks were also formed by the polysialic acid-containing carbohydrate units of N-CAM. The formation of filament bundles is a novel and unexpected property of polysialic acid and of short carbohydrate oligomers in general and represents a previously unrecognized molecular interaction mechanism which impacts both eukaryotic and prokaryotic cell-cell adhesions.

Biopolymers↗

PubMed1998

Cellular and molecular changes during sex differentiation of embryonic mammalian gonads.

Structural and molecular changes during sex differentiation and development of mammalian gonads from early embryonic phase until sexual maturity have been studied by morphologic and immunocytochemical methods in vivo and in experimental culture. The strategy has been to identify cellular macromolecules whose genes are differently expressed in the two sexes and to formulate a hypothetical regulatory chain of sex determination. This approach should provide new possibilities for finding the missing links between the final structural genes and the early regulatory genes, which are differentially expressed before and during gonadal differentiation. On the basis of accumulated structural and molecular evidence, the early epithelial differentiation from the precursor cells via cell aggregates to testicular cords or ovarian follicles is not sexually regulated. The biological consequences of sex determination in the differentiation of the genital organs include changes in the pattern formation of the gonadal epithelia and concomitant alterations in the synthesis and organization of the structural macromolecules.

Animals↗

PubMed1998

Differential distribution of type IV collagen chains in the developing rat testis and ovary.

The localization of type IV collagen alpha 1-alpha 5 chains in the differentiating rat testis and ovary was studied by immunocytochemistry. The initial formation of the testis and ovary included the appearance of collagen alpha 1/alpha 2(IV) chains in the gonadal blastemas. Upon further differentiation of the epithelia of the gonads alpha 1/alpha 2(IV) chains became localized in all of the respective basement membranes (BMs). The alpha 3, alpha 4 and alpha 5 chains of type IV collagen were not detectable in the prenatal rat testis and ovary. With the postnatal differentiation of the rat testis the alpha 3-alpha 5(IV) chains gradually appeared, and were localized in BMs of the testicular cords and seminiferous tubules, rete cords, myoid cells, surface epithelium, Leydig cells, and in some blood vessels. In the postnatal rat ovary, the alpha 3(IV) chain appeared in the BMs of small cortical follicles whereas the BMs of secondary and more deeply localized follicles were devoid of this chain. The alpha 1/alpha 2(IV) chains were abundant in the theca. A reaction for alpha 3-alpha 5(IV) chains also appeared in the BM of the ovarian surface epithelium and of some blood vessels after birth. The present results show that the alpha 3-alpha 5(IV) chains are not only less widely distributed than the alpha 1/alpha 2(IV) chains but are also synthesized much later in development. The late appearance of the alpha 3-alpha 5(IV) chains shows that the development of the mature testicular and ovarian BMs is a long process and that the time schedule for the synthesis of these chains is different from that of many other extracellular matrix proteins. A careful analysis of the expression of alpha 3(IV) chain may be useful in the further study of the kinetics and regulation of ovarian follicular growth.

Animals↗

PubMed1997

HLA-B27 modulates intracellular survival of Salmonella enteritidis in human monocytic cells.

Human major histocompatibility complex class I allele HLA-B27 is associated with a group of diseases called spondyloarthropathies. In reactive arthritis (ReA), the disease is triggered by certain infections, e.g. gastroenteritis caused by Salmonella. The host/microbe interaction is abnormal in susceptible individuals leading to inefficient elimination of arthritis-triggering bacteria, fragments of them, or both, after the initial infection. Using transfected human monocytic U937 cell lines, we demonstrate that the expression of the HLA-B27 antigen does not influence the uptake of S. enteritidis into U937 cells in vitro. Interestingly, HLA-B27 remarkably impairs the elimination of S. enteritidis within the HLA-B27 transfected U937 cells. The impaired elimination of ReA-triggering microbes by HLA-B27+ monocytes may offer an explanation for the persistence of ReA-triggering microbes in susceptible HLA-B27+ individuals. This modulation of the host/microbe interaction by HLA-B27 may have an important role in the pathogenesis of ReA.

Cell Count↗