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Results for “Neovascularization, Pathologic”

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PubMed2000

Matrix metalloproteinases and their natural inhibitors in fibrovascular membranes of proliferative diabetic retinopathy.

AIM: To examine epiretinal membranes of proliferative diabetic retinopathy (PDR) for the presence of selective matrix metalloproteinases (MMPs) and their natural inhibitors (TIMPs), in order to determine whether neovascularisation and fibrosis, characteristic of this complication of diabetes mellitus, are associated with specific anomalies of MMP or TIMP expression. METHODS: The presence of selected MMPs and TIMPs was investigated in 24 fibrovascular epiretinal membranes of PDR, and the findings compared with that observed in 21 avascular epiretinal membranes of proliferative vitreoretinopathy (PVR) and five normal retinas. Specimens were examined for deposition of interstitial collagenase (MMP-1), stromelysin-1 (MMP-3), gelatinase A (MMP-2), gelatinase B (MMP-9), and three tissue inhibitors of metalloproteinases (TIMP-1, TIMP-2, and TIMP-3). RESULTS: The results showed that unlike normal retina, which constitutively expresses MMP-1 and TIMP-2, a large proportion of PDR membranes (> 62%) stained for MMP-1, MMP-2, MMP-3, MMP-9, TIMP-1, TIMP-2, and TIMP-3. There were no differences in the expression of these molecules when compared with PVR membranes. A characteristic staining for MMP-9 was observed within the perivascular matrix of PDR membranes, and there was a significant increase in TIMP-2 expression by PDR membranes (p= 0.036) when compared with PVR membranes. CONCLUSIONS: The findings that MMPs involved in degradation of fibrovascular tissue matrix, as well as TIMP-1 and TIMP-2, are found in a large proportion of PDR membranes, and that their expression does not differ from that of PVR membranes, suggest the existence of common pathways of extracellular matrix degradation in pathological processes leading to retinal neovascularisation and fibrosis.

Diabetic Retinopathy↗

PubMed2004

[Change of vascular endothelial growth factor and its receptors expression in acute myeloid leukemia before and after treatment].

OBJECTIVE: To explore the role of angiogenesis in bone marrow in acute myeloid leukemia (AML). METHODS: Bone marrow culture supernatant was assayed for vascular endothelial growth factor (VEGF) by ELISA, bone marrow biopsies from 28 newly diagnosed AML patients were assayed for microvessel density (MVD), VEGF and its receptors KDR, Flt-1 by immunohistochemical staining before and after induction chemotherapy. RESULTS: Culture supernatant of AML bone marrow mononuclear cells showed higher amount of VEGF (425.31 ng/L) than that of control (140.12 ng/L). The VEGF and KDR expressions and MVD were significantly higher in newly diagnosed AML patients (78.6%, 78.6% and 7.1%, respectively) than that of control group (P < 0.05). There was a positive correlation between VEGF, KDR and MVD. The positive rate of VEGF, KDR and MVD reduced to normal after the patients achieved complete remission, while in non-remission patients did not. Kaplan-Meier analysis showed that the survival time was longer in VEGF negative group than in VEGF positive group. The pre-treatment MVD and VEGF had no correlation with survival time. CONCLUSIONS: There is remarkable angiogenesis in AML and VEGF/KDR signaling pathway takes an important role in the pathological angiogenesis. VEGF could be used as a prognostic factor in AML.

Adolescent↗

PubMed2004

Anti-angiogenic mechanisms and efficacy of the low molecular weight heparin, tinzaparin: anti-cancer efficacy.

Inhibitors of angiogenesis are potential anti-cancer agents in that they deprive tumors of the blood necessary for growth and metastasis. The anti-angiogenic efficacy of tinzaparin, a known anticoagulant low molecular weight heparin (LMWH), was examined in vitro in endothelial cell tube formation assay and in vivo in the chick chorioallantoic membrane model. The observed anti-angiogenic effects of tinzaparin were shown to be dose-related and dependent on the relatively higher molecular weight tinzaparin fragments. These experiments demonstrated that tinzaparin is a potent inhibitor of angiogenesis (ED90-100 range, 0.05-0.1 mg) regardless of the angiogenic factor and suggest that its effect is mediated via cellular release of tissue factor pathway inhibitor (TFPI). This was evident by the reversal of either tinzaparin or r-TFPI anti-angiogenesis efficacy by a specific monoclonal TFPI antibody. The ED90-100 for the inhibition of angiogenesis for r-TFPI ranged from 0.01 to 0.03 mg in the chorioallantoic membrane model regardless of the proangiogenic factor. In addition, either tinzaparin or r-TFPI inhibited the growth of colon carcinoma tumors, human fibrosarcoma tumors, and human lung carcinoma in the chorioallantoic membrane tumor implant model. Thus, the LMWH tinzaparin, in addition to its anticoagulant effects, may offer important benefits in treatment of cancer and other disorders supported by pathologic angiogenesis.

Angiogenesis Inhibitors↗

PubMed1994

Normal and abnormal development of the blood-brain barrier.

The blood-brain barrier is responsible for the maintenance of the neuronal microenvironment. This is accomplished by isolation of the brain from the blood by the tight junctions that join endothelial cells in cerebral microvessels, and by selective transport and metabolism of substances from blood or brain by the endothelial cells. This review describes the growth and maturation of the brain vasculature, and the development of the special properties of the endothelia at the blood-brain interface. Evidence suggests that the development of the unique properties of the brain microvasculature is a consequence of tissue-specific interactions between endothelial cells of extraneural origin and developing brain cells. The cellular and molecular mechanisms that control these processes are as yet unknown but this review will include experimental studies which have used in vivo and in vitro systems to investigate what factors may be involved, and some pathological conditions in which abnormal barrier development is thought to be an important aspect of the disease process.

Animals↗

PubMed1999

Evidence for 12-lipoxygenase induction in the vessel wall following balloon injury.

OBJECTIVE: Vascular smooth muscle cell (VSMC) migration and proliferation are key events in the development of atherosclerosis and restenosis following angioplasty. These events are mediated by several growth factors and cytokines whose cellular effects include activation of phospholipases and arachidonic acid metabolism via the lipoxygenase (LO) pathway. Since 12-LO products have potent growth and chemotactic effects, we have examined if 12-LO is upregulated in the neointima of injured rat carotid arteries and also if LO inhibition could attenuate neointimal thickening. METHODS: The left common carotid arteries of male Sprague Dawley rats were injured using a 1.8 F PTCA balloon catheter. Four-fourteen days after injury, injured and uninjured tissue samples were processed for histology, and immunohistochemistry or polymerase chain reaction (PCR) to examine 12-LO expression. RESULTS: Twelve days after injury, immunohistochemical staining with a 12-LO antibody revealed intense staining in injured left carotid arteries, mainly in neointimal VSMCs and inflammatory cells, but not in the uninjured right arteries. There was also a marked upregulation of 12-LO mRNA (over five-fold by competitive PCR) in the injured arteries. Treatment of the arteries with a LO inhibitor, phenidone, soon after injury resulted in significant inhibition of neointimal thickening. In contrast, a cyclooxygenase inhibitor, ibuprofen, had no effect. CONCLUSIONS: These results indicate for the first time that balloon injury results in marked induction of 12-LO mRNA and protein expression in the vessel wall. Furthermore, LO pathway activation may mediate, at least in part, the development of the lesion or plaque instability, suggesting a novel target for therapeutic intervention to block these pathological events.

Analysis of Variance↗

PubMed2003

[Tissue engineering: a tool to understand the physiological mechanisms].

Tissue engineering is a new domain, which allows some very unique studies of many human physiological mechanisms. This technology, based on cell capacity to reproduce a three-dimensional tissue with or without the help of biomaterials, is an interesting approach to study cells in an environment quite similar to the in vivo context. This article summarizes the LOEX's (laboratory of experimental organogenesis) scientific endeavor in tissue engineering in order to better understand some physiological or pathological mechanisms. Thus wound healing, stem cells, graft vascularization and cell interactions are domains where tissue engineering has already made a significant impact.

Cell Communication↗

PubMed2006

ICS-283: a system for targeted intravenous delivery of siRNA.

ICS-283 was developed within Intradigm Corporation as a system that is designed for the systemic delivery of therapeutic small interfering (siRNA) to sites of pathological angiogenesis. The non-viral siRNA delivery system is based on synthetic nanoparticles, known as Targe (Intradigm Corporation), which functions as a broad-platform technology to deliver siRNA to specific target cells in diseased tissues. The system is constructed to incorporate different functionalities that address critical needs for successful nucleic acid delivery. The TargeTran synthetic vector is a self-assembling, layered nanoparticle that protects and targets siRNA to specific cell types in pathological tissues. At present, ICS-283 is the only antiangiogenic siRNA delivery system that is designed for intravenous administration to treat angiogenesis-driven diseases.

Animals↗

PubMed2005

Senescence and its bypass in the vascular endothelium.

Vascular endothelial cells line the interior of blood vessels. As in other cell types, the proliferative lifespan of endothelial cells is limited; after a given number of replication cycles, they undergo senescence. Angiogenesis, the formation of new capillaries from pre-existing vasculature, is a process that involves endothelial cell proliferation. Angiogenesis thus has the possibility to be limited by the occurrence of senescence in the endothelial cell population. While there is evidence that endothelial cells undergo senescence in vivo, there are also data implying that endothelial senescence can be delayed or prevented in certain situations. Such a prevention of senescence would allow continued endothelial cell proliferation and continued angiogenesis in both physiological and pathological settings. This review discusses endothelial cell senescence and its bypass in vitro and in vivo.

Animals↗

PubMed1981

[Biology of the femoral head necrosis. Clinical studies (author's transl)].

From the study of femoral heads either experimental or human it is clear that the clinico-pathological called idiopathic necrosis is due to the death of bone cells, as it is in necrosis after fracture or dislocation. But the cause of cell's death is clearly avascular only in traumatic necrosis: in idiopathic necrosis there is no evidence of arterial alteration or obliteration, whatever condition is associated. In both avascular (traumatic) necrosis, and idiopathic necrosis, the cartilage remains alive: the deformation of the head, secondary rupture and destruction of cartilage and finally osteoarthritis are the consequence not of the death of bone cells (a dead head with living cartilage would work for along time) but of the revascularisation process. This process is different in the two syndrome. In idiopathic necrosis proliferation of living tissues in the head is active, but bone formation is limited, shearing forces create a subchondral fracture in the dead part of the head. In avascular necrosis, after the fracture is united, proliferation invades the dead head, with active osteogenesis. The pathological fracture is between dead and bone and revascularised part of the head. One can suggest as therapeutic measure the prevention of revascularisation.

Cell Survival↗

PubMedDate not supplied

Isolated capillary proliferation in Leigh's syndrome.

An infant with hypotonia and recurrent apneic spells died with a diagnosis of pyruvate dehydrogenase deficiency and showed typical pathological changes of Leigh's syndrome at postmortem. Despite the prominence of symptoms suggesting dysfunction of brainstem respiratory centers during life, lesions were not found in the upper medulla. However, quantitative morphometric analysis demonstrated abnormal capillary hyperplasia in the region including and between the nucleus ambiguus and nucleus tractus solitarius. There was an average area of 8.0 +/- 2.5 x 10(6) mm2 occupied by capillaries per 0.75 mm2 field in the patient's brainstem, compared with 4.6 +/- 1.6 x 10(6) mm2 and 5.5 +/- 1.4 x 10(6) mm2 in two age-matched controls (p < 0.01). We speculate that capillary hyperplasia is a pathological marker of chronically impaired oxidative metabolism in the central nervous system in metabolic disease.

Brain↗

PubMed2000

Photodynamic therapy for neovascular age-related macular degeneration.

BACKGROUND: In neovascular age-related macular degeneration, new vessels grow under the retina, distorting vision and leading to scarring. This is further exacerbated if the blood vessels leak. Photodynamic therapy, originally used in cancer treatment, has been investigated as a way to treat the neovascular membranes without affecting the retina. OBJECTIVES: The aim of this review is to examine the evidence for the safety and effectiveness of photodynamic therapy in the treatment of neovascular age-related macular degeneration. SEARCH STRATEGY: We searched for trials in the Cochrane Eyes and Vision Group trials register (available in the Cochrane Controlled Trials Register), the Cochrane Controlled Trials Register, Medline and Embase. We used the Science Citation Index to search for reports that cited identified relevant study reports. We contacted experts in the field for further trials information, and we searched the reference lists of identified relevant studies for further trial reports. Searches were conducted in December 1999. SELECTION CRITERIA: We included randomised trials of photodynamic therapy in people with choroidal neovascularisation due to age-related macular degeneration. DATA COLLECTION AND ANALYSIS: Two reviewers extracted the data independently. Meta analysis was not performed. MAIN RESULTS: One published trial was identified. Outcome data were available at 12 months after the first treatment. Patients received an average of 3.7 treatments. The relative risk of losing three or more lines of visual acuity at 12 months comparing the intervention with the control group was 0.72 (95% confidence interval 0.61 to 0.86). The relative risk of losing six or more lines of visual acuity at 12 months comparing the intervention with the control group was 0.62 (95% confidence interval 0.44 to 0.87). Subgroup analyses suggest that the benefits may be confined to people with no occult choroidal neovascularisation. REVIEWER'S CONCLUSIONS: Photodynamic therapy in people with classic choroidal neovascularisation due to age-related macular degeneration is effective in preventing visual loss. This evidence is drawn from a subgroup analysis of 143 participants in one trial. Outcomes and potential adverse effects of this treatment should be monitored closely. There is no evidence that photodynamic therapy is beneficial for people with evidence of occult choroidal neovascularisation. These people should be offered treatment in the context of a randomised trial.

Humans↗

PubMed2006

Heterogeneity in the remodeling of aneurysms of the ascending aorta with tricuspid aortic valves.

OBJECTIVES: The study addresses mechanisms driving the formation of ascending aortic aneurysms by comparing the maximal dilatation area with the transition area immediately adjacent to the normal aortic tissue left in place during surgical repair. METHODS: Aortic wall specimens were taken from the maximal dilatation area and transition area in 10 patients undergoing surgery for ascending aortic aneurysms and fixed for histology and immunohistochemistry for vascular smooth muscle cells (alpha-actin), endothelial cells (CD31), and macrophages (CD68). Tissue concentrations of vascular endothelial growth factor, matrix metalloproteinase-2, and matrix metalloproteinase-9 were determined by enzyme-linked immunosorbent assay. The results are expressed as medians with their 25th and 75th centiles. RESULTS: Vascular smooth muscle cells were significantly more abundant in the maximal dilatation area than in the transition area (20.3 [14.8-24.4]/10(-2) mm2 vs 8.0 [6.4-9.3]/10(-2) mm2, respectively, P = .002). In the maximal dilatation area, vascular smooth muscle cells had lost their typical lamellar organization, whereas it was preserved in the transition area. Microvessels were significantly more abundant in the media of transition area than in the maximal dilatation area (7.5 [2.9-10.1]/mm2 vs 1.75 [1.5-2.0]/mm2, respectively, P = .008) and were associated with an inflammatory cell infiltration that predominated in their immediate vicinity. There were no significant differences in vascular endothelial growth factor, matrix metalloproteinase-2, and matrix metalloproteinase-9 between both areas. CONCLUSIONS: The transition area appears as a disease progression front characterized by microvessel formation and inflammatory cell infiltration. In contrast, increased vascular smooth muscle cell density in the maximal dilatation area suggests a healing process, although inefficient to prevent aortic dilatation.

Actins↗

PubMed1999

Transvaginal color Doppler for predicting pathological response to preoperative chemoradiation in locally advanced cervical carcinoma: a preliminary study.

To evaluate the role of transvaginal color Doppler ultrasonography (TCD) in predicting pathological response to preoperative chemoradiation in patients with locally advanced cervical cancer, 10 patients (mean age: 45.2 y, range: 31 to 75 y) with histologically proven locally advanced cervical cancer who were scheduled for preoperative chemoradiation were evaluated by TCD prior to beginning the treatment protocol. Tumor volume, number of vessels within the tumor, lowest resistance index (RI), maximum peak systolic velocity (PSV), and the ratio between the number of vessels and tumor volume (tumor vascular density, TVD) were calculated. All patients underwent preoperative chemoradiation and radical surgery. Complete pathological response (pathCR) was considered when no residual tumor was found on surgical specimens. Partial pathological response (pathPR) was considered when residual tumor was found. PathCR was achieved in three patients (30%), whereas 7 (70%) had pathPR. Mean tumoral volume was not statistically different between those with pathCR (33.2 cm3) and those with pathPR (20.3 cm3) (p = 0.305). Those tumors with pathCR had lower mean number of vessels (3.3 vs. 5.3, p = 0.01), lower TVD (0.1 vs. 1.1, p = 0.05) and higher RI (0.41 vs. 0.29, p = 0.03). No differences were found in PSV. Although these data are preliminary, our results suggest that TCD may be used to predict pathological response to preoperative chemoradiation in patients with locally advanced cervical cancer.

Adenocarcinoma↗

PubMed2006

18-Fluorine-labelled 2-deoxy-2-fluoro-D-glucose positron emission tomography/computed tomography standardised uptake values: a non-invasive biomarker for the risk of metastasis from choroidal melanoma.

AIMS: To correlate the clinical, ultrasound and pathological features of the eyes first evaluated by 18-fluorine-labelled 2-deoxy-2-fluoro-d-glucose (FDG) positron emission tomography (PET)/computed tomography and then enucleated for choroidal melanoma. METHODS: 14 consecutive patients enucleated for choroidal melanoma were examined. At presentation, clinical, ultrasound and PET/computed tomography imaging were carried out. Ultrasound was used to measure the tumour size and evaluate the tumour shape and intrinsic vascularity (blood flow). Histopathological and immunohistochemical evaluations included tumour cell type, necrosis, glycogen content, vascularity and extrascleral extension. RESULTS: 13 tumours were T3 and one T2 (American Joint Committee on Cancer - International Union against Cancer). The mean tumour height was 10.6 (range 3.5-17.7) mm with a largest basal dimension of 19.3 (range 14.5-30) mm. Patients having melanoma with the highest six standardised uptake values ((SUV) > or =4.0) were (on average) >10 years older, their melanomas had larger basal dimensions and were epithelioid-cell type; three melanomas were centred anterior to the equator; three contained enlarged blood vessels (>150 mum in diameter); and three formed extrascleral extension. Patients with the two highest SUV tumours died due to metastatic melanoma. CONCLUSION: PET/computed tomography imaging offers a physiological assessment of glucose metabolism in primary choroidal melanomas. Increased FDG PET/computed tomography SUV was positively correlated with known clinical, pathological and ultrasound features linked to metastatic potential of choroidal melanoma.

Adult↗

PubMed2005

Regulation of the pathological vasculature of malignant astrocytomas by angiopoietin-1.

Malignant astrocytomas are the most common and highly vascularized of all primary adult brain tumors. The histopathological hallmarks of malignant astrocytomas are microvascular proliferation and formation of vascular entities, which are referred to as "glomeruloid bodies." The significance of glomeruloid bodies and the molecular mechanisms driving the abnormal vascular architecture in malignant astrocytomas are not understood. We have observed that overexpression of angiopoietin-1 (Ang1) in both subcutaneous and intracranial xenograft models of malignant astrocytomas reproduces many of the vascular features of these tumors, including glomeruloid bodies. To confirm that the formation of glomeruloid bodies was directly dependent on Ang1, we performed experiments where levels of Ang1 expression were regulated under tetracycline control, and we found a direct correlation between levels of Ang1 expression and the occurrence of glomeruloid bodies in xenografts. Additionally, we inhibited the action of Ang1 by blocking its cognate receptor Tie2, and we found that the formation of glomeruloid bodies was inhibited. Collectively, these results support our hypothesis that Ang1 is a key molecular regulator of pathological vascularization characteristic of malignant astrocytomas.

Angiogenesis Inducing Agents↗

PubMed2002

Correlation between color power Doppler sonographic measurement of breast tumor vasculature and immunohistochemical analysis of microvessel density for the quantitation of angiogenesis.

OBJECTIVE: To record the correlation between color power Doppler sonographic measurement of breast tumor vasculature and immunohistochemical analysis of microvessel density for the quantitation of angiogenesis. METHODS: Women with palpable breast masses scheduled for excision biopsy were scanned with two- and three-dimensional color power Doppler sonography before and after the administration of a sonographic contrast agent. Vessel counts were performed on two- and three-dimensional sonographic images before and after contrast agent administration. All tumors were surgically removed and underwent immunohistochemical analysis for microvessel density assessment. The sonographic measure of tumor vascularity was correlated with microvessel density. RESULTS: Pathologic examination showed 43 breast cancers and 14 benign breast masses. Higher microvessel density was noted in malignant than benign breast masses (P < .0005). Color power Doppler sonographic measurement of tumor vessel number showed a significant positive correlation with tumor size (P < .05) and progesterone receptor negativity (P < .05). A significant positive correlation was observed between microvessel density and the number of intratumoral blood vessels assessed by both two- and three-dimensional color power Doppler sonography (P < .05). Regression models showed three-dimensional color power Doppler sonography to have a significantly higher correlation with microvessel density when compared with two-dimensional color power Doppler sonography at baseline (P < .005). The administration of a sonographic contrast agent did not improve correlation with microvessel density. CONCLUSIONS: A significant correlation was shown between color power Doppler sonographic measurement of tumor vascularity and microvessel density by immunohistochemical analysis. Further improvement in Doppler sonographic techniques to map capillary vessel flow should be explored to improve the current association with pathologic findings.

Adult↗

PubMed2002

Role of color flow Doppler sonography in pre-operative diagnostics of the thyroid pathology.

BACKGROUND: The aim of this work is to demonstrate the high effectiveness of preoperative diagnosis by echotomographic study of thyroid nodules through color-Doppler sonography integrated by B-mode. The authors performed both B-mode ultrasonography and color-Doppler sonography on 125 patients expecting total thyroidectomy surgical intervention, without a previous evaluation of a number of other already performed clinical and instrumental tests. After the intervention, we compared the histologic test with the data drawn from the ultrasound scan, in order to demonstrate that color-Doppler sonography is able to provide for additional diagnostic information in the preoperative period. METHODS: One hundred and twenty five patients with thyroid pathologies were examined by both B-mode and color-Doppler sonography. Two diagnoses were made for each clinical case: the first supported by B-mode data, the second based on vascularity. Our aim was to check color-Doppler's ability to provide new information in the ultrasound diagnosis. All patients underwent a total thyroidectomy surgical intervention. The data were examined by K concordance test. RESULTS: Ultrasound data were compared with the histologic test, which showed 118 (97.4%) benign and 7 (5.6%) malignant lesions. B-mode ultrasound test gave a correct diagnosis in 115 (97%) out of 118 benign lesions and in 4 (57%) out of 7 malignant lesions, while 3 (2.5%) out of 118 cases were false positive and 3 (42.8%) out of 7 were false negative. In those cases showing a wrong conventional ultrasound diagnosis, after the integration of B-mode with color-Doppler results, a decrease was recorded in both false negative and false positive. CONCLUSIONS: Even if no correspondence was found between the different aspects of blood flow and the histologic types of lesions, this experience proves that the color-Doppler test has a high predictive value of benignity in cases with pattern I II and IV, while lesions with pattern III should be more carefully examined, since both malignant and benign lesions belong to this group. From the data drawn from this study, we are able to infer that color-Doppler sonography is undoubtedly an advantage not only in terms of cutting the false negatives, but also in the aim of obtaining a higher effectiveness in the screening of goitrogenic pathology.

Adenocarcinoma, Follicular↗

PubMed1994

Transforming growth factor-beta 1 mediates mast cell chemotaxis.

It remains unknown which factor(s) control mast cell recruitment in chronic immune reactions. Although TGF-beta has been shown to function as a potent chemotactic factor for monocytes, fibroblasts, and neutrophils, its effect on mast cells has not been previously determined. In this study, TGF-beta 1 was shown to cause directed migration of cultured mouse mast cells at femtomolar concentrations, with a maximal chemotactic response observed at 25 fM. Moreover, chemotaxis to TGF-beta was also seen using freshly isolated rat peritoneal mast cells. Addition of neutralizing Ab to TGF-beta abrogated its chemotactic activity for both freshly isolated rat peritoneal mast cells and cultured mouse mast cells, whereas an irrelevant species-matched control Ab had no effect. Checkerboard analysis confirmed the mast cell chemotactic activity after exposure to concentration gradients of TGF-beta. Mast cells were observed to undergo rapid and extensive shape changes on exposure to TGF-beta, assuming a polarized morphology in preparation for migration. Other known mast cell chemoattractants including laminin, c-kit ligand, and IL-3 were found to be considerably less potent on a molar basis in inducing directed migration. Affinity cross-linking studies identified TGF-beta binding proteins with M(r) at 70 and 288 kDa, consistent with types I and III TGF-beta receptors on the mast cells. In summary, TGF-beta is the most potent chemoattractant described for mast cells and conceivably relevant, because pathologic processes mediated by TGF-beta are often associated with mast cell accumulation.

Animals↗