[Uses of autologous stem cell transplantation in the field of burns and injuries].
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Burns↗
Biomedical subjects
Xiao-bing Fu
Publications and source records attributed to Xiao-bing Fu.
[Relationship between epithelial-immunologic cells transdifferentiation and pseudoepitheliomatous granuloma lesion].
OBJECTIVE: Inappropriate treatment at early stage of wound could result in the formation of pseudoepitheliomatous granuloma (PEG). The correlation of abnormal transdifferentiation of epithelial cells to immunologic cells and the occurrence of PEG lesion was investigated. METHODS: Morphological change of epithelial tissue was observed with histopathology in 11 specimens of PEG lesions and 6 specimens of normal skins from PEG edge (PEG-N) from 11 patients with damaged skin. The expression characteristics and distribution of pan-cytokeratin (CKp), IV type collagen, laminin (LM), epithelial cadherin (E-Cad), beta-catenin (beta-Cat), focal adhesion kinase (FAK), stem cell factor (SCF) and its receptor-c-Kit, proliferating cell nuclear antigen(PCNA), and cluster of differentiation-14 (CD14), CD68 and mast cell tryptase (MCT) in PEG were detected with the immunohistochemical and the indirect immunofluorescent double-staining. RESULTS: In comparison with PEG-N, epithelial tissue take on squamous metaplasia, and stroma was infiltrated with intensive microvessels and inflammatory cells in the PEG lesion. Poor epithelial basal layer constitution, basal polarization, and migration of basal cells to stroma could be observed. In the ultrastructure, the loose intercellular junction of basal cells and the increased nucleus/cytoplasm ratio and intercellular space could be observed, neonatal monocytoid cells and macrophages and mast cells as a exuviate-like manner brooded from cytoplasm of original epithelial cells and basement membrane. protein expression of CKp and E-Cad by basal cells was significantly decreased, and the IV type collagen and LM protein could not be found in basement membrane of identical locus. By contrast, the immunoreactivity of beta-Cat and FAK was apparently increased. In addition, CD14(+) monocytes, CD68(+) macrophages, MCT(+) mast cells and CD68(+)/MCT(+) cells with various size, and these cells of stronger immuno-staining of SCF, c-Kit and PCNA antigen could be found in epithelial tissue and stroma. CONCLUSION: Epithelial cells in PEG related to wound are characteristized by transdifferentiation of epithelial cells to immunologic cells, wich may be associated with local infectious and inflammatory reaction, ultimately resulting in enhancement the ratio of beta-Cat/E-Cad signal and activation SCF-c-Kit signal pathway. The phenomena of transdifferentiation epithelial cells in the PEG lesion will help to recognize of the neoplatic immune and trauma repair mechanism.
Adolescent↗
[Effects of acute hypoxia and intermittent hypoxic acclimatization on erythropoietin and hypoxia-inducible factor-1alpha gene expression in rat hepatic and renal tissues].
OBJECTIVE: To explore the effects of acute hypoxia and intermittent hypoxic acclimatization on gene expression of erythropoietin (EPO) and hypoxia-inducible factor-1alpha (HIF-1alpha) in rat hepatic and renal tissues. METHODS: Twenty-four rats (weight was 180 to 220 g) were divided into three groups: normal control group (NC), intermittent hypoxic acclimatization (IH) and acute hypoxia groups (AH). Gene expression of EPO and HIF-1alpha were examined with Northern dot blot method. RESULTS: As compared with NC group, the levels of EPO gene expression in rat hepatic and renal tissues in AH group were both significantly elevated (P<0.05 or P<0.01). In IH group, the contents of EPO mRNA in hepatic and renal tissues were apparently decreased versus AH group (P<0.01), whilst were not differently elevated in comparison with group NC (P>0.05). In hepatic tissue from AH group, the content of HIF-1alpha mRNA were more than those in NC group and IH group, while the levels of gene expression of HIF-1alpha were no substantial change in renal tissues from different groups (all P>0.05). CONCLUSION: Hypoxic acclimatization can inhibit the increment of EPO gene expression induced by acute hypoxia in rat hepatic and renal tissues, in which HIF-1alpha may play important roles.
Adaptation, Physiological↗
[Effects of fibroblast growth factor-10 on the secretions of transforming growth factor-alpha, platelet-derived growth factor-AB and vascular endothelial growth factor by normal adult human keratinocytes in culture].
OBJECTIVE: To evaluate the effect of fibroblast growth factor-10 (FGF-10) on the secretion of transforming growth factor-alpha (TGF-alpha), platelet-derived growth factor-AB (PDGF-AB) and vascular endothelial growth factor (VEGF) by human keratinocytes. METHODS: Concentrations of FGF-10 used were 4, 16, 125 and 500 ng/ml. Serum-free keratinocyte growth medium without EGF or with EGF were as negative control and positive control, respectively. Cells were cultured at 2500, 37500 cells/cm 2 in dishes in serum-free medium and supernatants were collected at 24, 48 and 72 hours. The concentrations of TGF-alpha PDGF-AB and VEGF in cell culture supernatant were measured by using TGF-alpha, PDGF-AB and VEGF enzyme linked immunoadsorbent assay (ELISA) kits, respectively and cell numbers were counted by haemocytometer. RESULTS: For cells cultured at low density and cells were subconfluent, TGF-alpha in each group was low and there was no significant difference among them at 24 hours. At 48 hours, both in absolute concentrations and on a per-cell basis, FGF-10 enhanced the secretion of TGF-alpha by cells cultured at low density in a dose-dependent fashion. At 72 hours, the concentrations of TGF-alpha in all dose of FGF-10 were significantly higher than that in negative control (P<0.05). The production of TGF-alpha in pg/10(6) cells in 500 ng/ml FGF-10 reached statistical significance compared with negative control (P<0.05). The secretion of TGF-alpha in FGF-10 were lower than that in positive control at 48 and 72 hours. For cells cuttured at 37500 cells/cm(2), the secretion of TGF-alpha stimulated by FGF-10 was similar to that when cells cuttured at lower density. PDGF-AB in each group was undetectable. When cells cuttured at high density and reached 100 percent confluent, PDGF-AB could not be detected at 24 hours. At 48 hours, both in absolute concentrations and on a per-cell basis, PDGF-AB productions in 125 and 500 ng/ml of FGF-10 were markedly greater than those of negative control at 48 and 72 hours (P<0.05), and the secretion of PDGF-AB stimulated by FGF-10 was in a dose-dependent fashion. For cells cultured at low density, although the concentrations of VEGF in 16-500 ng/ml of FGF-10 were significantly higher than that in negative control (P<0.05) at 72 hours, on a per-cell basis, they were not greater than that of negative control. The secretion of VEGF in positive control was greater than that of FGF-10 at 24-72 hours. CONCLUSION: The effect of FGF-10 on increasing secretion of TGF-alpha and PDGF-AB might mediate the actions of FGF-10 on keratinocytes, fibroblasts and endothelial cells to promote re-epithelialization as well as granulation tissue deposition during wound healing.
Cells, Cultured↗
[Effects of acidi fibroblast growth factor on hepatic and renal functions after intestinal ischemia/reperfusion injury].
OBJECTIVE: To investigate the change in hepatic and renal functions parameters after intestinal ischemia-reperfusion (I/R) injury, and to explore the effects of acidic fibroblast growth factor (aFGF) on hepatic and renal functions after intestinal I/R injury in rats. METHODS: Seventy-eight Wistar rats were divided into four groups, which are sham-operated (C) group, ischemia (45 minutes) plus reperfusion (R), reconstructive human aFGF treatment (rhF), and wild type aFGF treatment (wtF) groups. The animals were sacrificed at 2, 6, 12 and 24 hours, respectively. Hepatic and renal functions were analyzed. RESULTS: In comparison with those in group C, the hepatic and renal functions were damaged in group R, rhF and wtF decreased. Treatment with rhF and wtF markedly abated the hepatic and renal dysfunction. The desquamation of intestine villi and infiltration of inflammation cells in the submucosa were observed in all groups. CONCLUSION: Hepatic and renal functions are damaged after intestinal I/R injury. Treatment with rhF and wtF could protect against multiple organ dysfunction associated with intestinal ischemia-reperfusiun injury.
Animals↗
[Study of mechanism on loss of some components from basement membrane in epithelial-interstitial junction in cutaneous pseudoepitheliomatous hyperplasia lesion].
OBJECTIVE: To investigate the relationship between the formation of pseudoepitheliomatous hyperplasia (PEH) and the mechanism of loss of some components from the basement membrane in epithelial interstitial junction (EIJ) in the treatment of cutaneous wounds, when formation of PEH lesion was induced. METHODS: Morphological change in epithelial tissue was observed with histopathologic method and electronic microscopy in 11 specimens of PEH lesions and 6 specimens of normal skin adjacent to PEH (PEH-N) from 11 patients with injured skin. The expression characteristics and distribution of pan-cytokeratin (p-CK), matrix metalloproteinase-2 (MMP-2), MMP-3, MMP-9, proliferating cell nuclear antigen (PCNA), epithelial cadherin(E-Cad) and beta-catenin(beta-Cat) in EMJ were detected with immunohistochemical methods. RESULTS: Epithelial cells expressing P-CK presented squamous epithelialization and extended into deep layer of mesenchyma. In epithelium-mesenchyma junction, where IV type collagen and laminin were weakly expressed, the protein contents of p-CK, E-Cad, MMP-2, MMP-3 MMP-9 were decreased, whilst the immunochemical staining of beta-Cat and PCNA was apparently increased. In the junction, epithelial basal cells were observed to migrate and to depart from basal membrane; epithelial islands and isolated epithelial cells expressing p-CK in mesenchyma could be observed. Ultrastructural observation revealed deformation of epithelial basal cells, increment of nucleus/cytoplasm ratio, loosened intercellular junctions, decrement of electronic density of BM and derangement of BM structure could be observed. CONCLUSION: Reduction in the capability of epithelial basal cells adhesion, differentiation and formation of basement membrane and cytokeratin in PEH associated with wound may be the crucial cause which controls epithelial cells migration into mesenchyma. That the contents of ColIV and LN were decreased may not be associated with MMPs, but with enhancement of the ratio of beta-Cat/E-Cad signal might be the important mechanism of dedifferentiation of epithelial basal cells and the loss of ability of structure formation and cellular migration.
Basement Membrane↗
[Gene expression of stress activated protein kinase and its MAPKs in hypertrophic scar].
OBJECTIVE: To explore the change of gene expression of stress activated protein kinase (SAPK) and its upstream signal-regulated molecule--mitogen activated protein kinases(MAPKs) (MKK4 and MKK7) in hypertrophic scar and auto-control normal skin. METHODS: The total RNA was isolated from 8 hypertrophic scars and 8 auto-control skin, and then mRNA was purified. The gene expressions of MKK4, MKK7 and SAPK were examined with reverse transcription-polymerase chain reaction(RT-PCR) method. RESULTS: In hypertrophic scar, both MKK7 and SAPK genes weakly expressed. In auto-control skin, the expression of these 2 genes was significantly elevated in comparison with hypertrophic scar (P < 0.01). The expression levels of these 2 genes were 1.5 times and 2.6 times as long as those of hypertrophic scar, respectively. Gene expression of MKK4 had no significant difference between auto-control skin and hypertrophic scar (P > 0.05). CONCLUSION: Decreased gene expression of MKK7 and SAPK which results in reducing cell apoptosis might be one of the mechanisms for controlling the formation of hypertrophic scar.
Adolescent↗
[Expression characteristics of transforming growth factor-beta1 in human skin at different development stages of gestation].
OBJECTIVE: To investigate gene expression of transforming growth factor-beta(1) (TGF-beta(1)) and its two upstream signalling factors (smad2 and smad3) in fetal skin at different gestational ages and postnatal skin and its potential biological significance. METHODS: Fetal skin samples of human embryo were obtained from spontaneous abortions at different gestational ages ranging from 13 to 32 weeks, and also skin collected from patients undergoing plastic surgery. After morphological characteristics of skin at different developmental stages were examined histologically, gene expressions of TGF-beta(1), smad2 and smad3 in skin specimens at different developmental stages were examined with reverse transcription-polymerase chain reaction analysis (RT-PCR). RESULTS: Gene expression of TGF-beta(1), smad2 and smad3 could all be detected in fetal skin and skin after birth. In skin from early gestational fetus, gene expressions of TGF-beta(1) and smad2 were weak. Along with advance in gestational age, gene expression of these two genes in skin became progressively stronger. In skin from late gestational fetus and skin after birth, the transcription contents of these two genes were significantly increased compared with early gestation fetus (P<0.05). On the contrary, gene expression of smad3 was apparently higher in younger fetal skin versus elder compared with that of late fetal skin (P<0.05). In skins after birth, the levels of smad3 gene expression were elevated to the level similar to that in early gestational fetal skin. CONCLUSION: The signal pathway mediated by TGF-beta(1) might be involved in regulating development of the skin at embryonic stage and in designating cetaceous structure and function, and also in wound healing after birth. The relative lack in expression of TGF-beta(1) and smad2 genes in skins from younger fetuses might contribute to fetal scar-less healing, in which the role of smad3 needs to be further investigated.
Actins↗
Development of gene microarray in screening differently expressed genes in keloid and normal-control skin.
BACKGROUND: Keloid is an intricate lesion that is probably regulated by many genes. In this study, the authors used the technique of complementary DNA (cDNA) microarray to analyse abnormal gene expression in keloids and normal control skins. METHODS: The polymerase chain reaction (PCR) products of 8400 genes were spotted in an array on chemical-material-coated-glass plates. The DNAs were fixed on the glass plates. The total RNAs were isolated from freshly excised human keloid and normal control skins, and the mRNAs were then purified. The mRNA from both keloid and normal control skins were reversely transcribed to cDNAs, with the incorporation of fluorescent dUTP, for preparing the hybridisation probes. The mixed probes were then hybridised to the cDNA microarray. After thorough washing, the cDNA microarray was scanned for differing fluorescent signals from two types of tissues. Gene expression of tissue growth factor-beta1 (TGF-beta1) and of c-myc was detected with both RT-PCR and Northern blot hybridisation to confirm the effectiveness of cDNA microarray. RESULTS: Among the 8400 human genes, 402 were detected with different expression levels between keloid and normal control skins. Two hundred and fifty genes, including TGF-beta1 and c-myc, were up-regulated and 152 genes were down-regulated. Higher expressions of TGF-beta1 and c-myc in keloid were also revealed using RT-PCR and Northern blot methods. CONCLUSION: cDNA microarray analysis provides a powerful tool for investigating differential gene expression in keloid and normal control skins. Keloid is a complicated lesion with many genes involved.
DNA, Complementary↗
[Analysis of etiological factors of pseudo-epitheliomatous granuloma after cutaneous wound healing: a report of 11 cases of patients with this lesion].
OBJECTIVE: To explore the pathogenetic mechanism, clinical and pathological characteristics, and prevention and treatment of pseudo-epitheliomatous granuloma after skin wound healing. METHODS: The clinical information and the treatment results of pseudo-epitheliomatous granuloma occurring in 11 patients (age 1-67 years) were reviewed and analyzed, their tissue specimens were used for microbial examination and histological observation. RESULTS: Some bacteria such as Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus hemolyticus B, and Streptococcus faecalis could be found in the culture of pseudo-epitheliomatous granuloma. The maJority of these bacteria was tolerant to celbenin but sensitive to vancomycin. The lesions were excised, and the wounds were covered with skin grafting or skin flap, supplemented by local of vancomycin to prevent recurrence of the lesion. Histological examination revealed in pseudo-epitheliomatous granuloma with long epithelial peduncle encapsulating granulation tissue like honeycomb, in which there were many capillaries, macrophages, lymphocytes and mast cells, with only a small amount of extracellular matrix. CONCLUSION: The main pathogenesis of pseudo-epitheliomatous granuloma formation might be improper treatment of wound in earlier period and infection of drug resistant bacteria. Surgical debridement followed by skin coverage and local inJection of vancomycin could be effective and curative.
Adolescent↗
[Effects of reconstructive human acidic fibroblast growth factor and wild type acidic fibroblast growth factor on skin cell proliferation].
OBJECTIVE: To investigate the effects of reconstructive human acidic fibroblast growth factor (aFGF) and wild type aFGF on skin cell proliferation in rat. METHODS: Neonatal rat skin (area of 2 mmx2 mm) was cultured in Dulbecco's modification of Eagle's medium containing reconstructive human aFGF and wild type aFGF, respectively. The concentrations of aFGF were 1 microg/L, 10 microg/L, and 100 microg/L. After being cultured for 4 days, the area of skin was measured. RESULTS: After treatment with two different growth factors in three different concentrations (1 microg/L, 10 microg/L and 100 microg/L) for 4 days, the areas of skin in three reconstructive human aFGF groups were 1.4, 1.5 and 1.3 fold of that of control, respectively and the areas of three wild type aFGF groups were 1.5, 3.2 and 1.6 fold of that of control, respectively, while the area of skin in the control group was (2.96+/-1.12) mm(2). In comparison with those of other groups, the skin area of 10 microg/L wild type aFGF group was significantly increased (P<0.05). CONCLUSION: Reconstructive human aFGF confers less impact on cutaneous cell growth. The capability of wild type aFGF to induce cutaneous cell proliferation is much greater than that of reconstructive human aFGF.
Animals↗
[Effects of acidic fibroblast growth factor on intestinal mucosal damage due to ischemia/reperfusion].
OBJECTIVE: To investigate the effect of exogenous acidic fibroblast growth factor (aFGF) on ischemia/reperfusion (I/R) injury of the intestine in rat, and to explore the mechanism of its protective effect. METHODS: The model of rat intestinal I/R injury was replicated by clamping the superior mesenteric artery (SMA) for 45 minutes followed by reperfusion. Seventy-eight Wistar rats were divided randomly into sham-operation group, intestinal I/R control group and aFGF treated group. In sham-operation group, SMA were separated but not occluded. Animals were sacrificed, samples of blood and tissue from the intestine were obtained 45 minutes after ischemia in sham-operation group and 0.5, 1, 2, 6, 12, and 24 hours after reperfusion in the other groups. Plasma D-lactate level was measured and rat survival rate was noted. Histological changes in intestinal tissue were observed under light microscope. RESULTS: The results showed that rat survival rate in aFGF treatment group was higher than that of intestinal I/R control group (P<0.05), and plasma D-lactate levels were markedly lower in aFGF group than that of intestinal I/R control group (P<0.05). Improvement in pathological changes was observed at 1, 2, 6, 12, and 24 hours after the reperfusion in aFGF treatment group compared with intestinal I/R control group. CONCLUSION: These data suggest that aFGF has a protective effect on intestinal I/R damage, and it may be related to the mitogenic effects and some hormone-like activities of aFGF.
Animals↗
[Relationship of overexpression of angiogenesis factors and their receptors with invasive growth of keloid].
OBJECTIVE: To study the relationship between invasive growth and the angiogenesis factors and their receptors in keloid. METHODS: Biopsies from 17 keloid (Ke) were divided into atrophy group (Ke-A, n = 9), proliferating group (Ke-P, n = 13), infiltrating group (Ke-I, n = 9), normal skin around Ke (Ke-N, n = 10) and normal skin (NS, n = 10). The histology, immunohistochemistry and computerized imaging analysis were used for the study. The levels of basic fibroblast growth factor (bFGF) and its receptor-Flg, vascular endothelial growth factor (VEGF) and VEGF/KDR complex (11B5), and platelet derived growth factor (PDGF-A) and its receptor-PDGFR-alpha, and alpha-smooth muscle actin (alpha-SMA) were determined in specimens with immuneohistochemical staining. RESULTS: In all 5 groups, bFGF, Flg, VEGF, 11B5, PDGF-A, and PDGFR-alpha were all expressed in fibroblasts (Fb), monocyte-phagocytes, vascular endothelial cells, adventitial cells, epidermal (cells and epithelial cells in appendage. The intensities of staining ranked as follows: Ke-I > Ke-N approximately equal to Ke-P > Ke-A approximately equal to NS, Flg > hFGF approximately equal to PDGFR-alpha > PDGF-A approximately equal to 11B5 > VEGF (P < 0.05 to approximately 0.01). 11B5 and VEGF were expressed (intensively in alpha-SMA positive myofibroblasts only in Ke-I group. The histological observation showed hyperplasia of endothelial cells and obliteration of microvessels. CONCLUSION: The invasive growth of keloid may be related to the overexpression of angiogenesis factors and their receptors. The abnormal expression of 11B5 in myofibroblasts may be one of the important factors associated with tumor-like growth feature in the invasive parts sites of keloid. The results suggest that inhibition of these biological activities would be of significance in clinical therapy.
Adolescent↗
[Gene expression of extracellular-signal regulated protein kinase 5 and their MAPKK in fetal skin hypertrophic scars].
OBJECTIVE: To explore the change of gene expression of extracellular-signal regulated protein kinase 5 (ERK5) and its upstream signaling molecule (MEK5) in fetal skin of differentially developmental stages and hypertrophic scars. METHODS: After morphological characteristics of skin of different developmental stages and hypertrophic scars were detected with pathological methods, gene expression of ERK5 and MEK5 was examined with reverse transcription-polymerase chain reaction analysis (RT-PCR). RESULTS: In early gestational fetal skin, genes of ERK5 and MEK5 were strongly expressed, while in late gestational skin and children skin, the expression of ERK5 and MEK5 was apparently decreased (P < 0.05). In normal skin, the level of gene expression of ERK5 was lower. In proliferative hypertrophic scars, mRNA content of this gene was apparently increased. In mature scars, the content of this gene transcript was 3.2 times the normal skin. In contrast, the levels of MEK5 transcript in normal skin and hypertrophic scars of various phases showed no substantial changes (P > 0.05). CONCLUSION: ERKS medicating signaling pathway might be involved in regulating cutaneous development at the embryonic stage and determining cutaneous structure ad function. The increase of gene transcription of ERK5 and MEK5 in younger fetal skin might be a reason for rapid proliferation of the skin cells and scraless healing of skin. The activation of ERK5 gene expression in hypertrophic scars versus normal skin might be one of the mechanisms controlling the formation of hypertrophic scars, in which the role of MEK5 needed to be further studied.
Child↗
[Study in the novel function of adipose tissue on wound healing].
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Adipose Tissue↗
[Redistribution of epidermal stem cells in wound edge in the process of re-epithelialization].
OBJECTIVE: To study the redistribution of epidermal stem cells in regenerating wound tissues, and to elucidate the role of epidermal stem cells during wound repair. METHODS: 80 circular full-thickness wounds were produced on both sides of the back in 20 male Wistar rats (4 wounds in each animal). Then the 80 wounds were randomly divided into 2 groups: group A (treated with sulfadiazine silver- sulfadiazine zinc cream, n = 40) and group B (without any treatment, n = 40). The infection and healing process of the wounds were observed with naked eyes. Five mice were killed one time 3, 7, 14, and 21 days after the wounding. Two wounds with surrounding normal skin tissues were collected from each mouse. Routine histological examination was conducted with HE staining. Beta(1) integrin and keratin19 (K19), markers of epidermal stem cells, were employed to determine the distribution of epidermal stem cells with streptavidin-peroxidase (SP) immunohistochemical method. RESULTS: The healing rate of wounds was 80% (32/40) in group A, and 60% (24/40) in group B. No beta(1) integrin and K19 positive cells was found in the granulation tissue of all wounds in these 2 groups at any time point during the healing process. However, a few beta1 integrin and K19 positive cells, bearing no anatomic relation with the epidermal stem cells in the basal layer, were found scattering in the stratum spinosum and stratum granulosum of the epidermis on the wound edges. The closer to the wound the more concentrated the beta(1) integrin and keratin19 positive cells. Their numbers increased gradually along with the shrinking of the wound surface until the wound completely healed. The numbers of the beta(1) integrin and keratin19 positive cells decreased gradually after epithelialization. The numbers of the beta(1) integrin and keratin19 positive cells were obviously lower in the infected wounds than in the uninfected wounds. CONCLUSION: Epidermal stem cells participated in the healing of wound. The function of redistribution of epidermal stem cells in wound edges seems to promote the re-epithelialization of granulating wounds.
Animals↗
Relationship between expression of Bax and Bcl-2 proteins and apoptosis in radiation compound wound healing of rats.
OBJECTIVE: To study the relationship between the expression of Bax, Bcl-2 proteins, and apoptosis in radiation compound wound healing of rats. METHODS: Apoptosis, Bax and Bcl-2 proteins were estimated by in situ terminal labeling (TUNEL) and immunohistochemical methods. RESULTS: (1) Changes of the apoptosis in wound healing showed three typical characteristics: early occurrence, high frequency and delayed disappearance after radiation to rats when compared with those of simple wound group, which might be an important reason for radiation-induced delayed wound healing. (2) The expression of Bax protein increased evidently with the increment of apoptosis and showed a good corresponding relationship with the apoptotic frequency in the process of wound healing. While the expression of Bcl-2 protein decreased obviously as the apoptosis reached a maximum and showed increasing tendency up to normal level when the apoptosis decreased distinctively. CONCLUSIONS: Bax and Bcl-2 proteins play an important role in the apoptotic regulation of radiation compound wound healing in rats.
Animals↗
[Gene expression of extracellular-signal regulated protein kinase 1/2 and their MAPKKs in hypertrophic scars].
OBJECTIVE: To explore the change of extracellular-signal regulated protein kinase 1/2 (ERK1/2) and their mitogen activated protein kinase kinases(MAPKKs) gene expression in normal skins versus hypertrophic scars underlying their biological significances. METHODS: After total RNAs were isolated from 8 specimens of hypertrophic scars and 8 specimens of normal skins, and then were purified to mRNAs, the gene expression of ERK1/2 and MEK1/2 were examined with reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: In normal skins, the intensity of gene expression of ERK1/2 and MEK1/2 were weak. In hypertrophic scar, the expression intensities of these 4 genes were 1.1 times, 1.2 times, 2.2 times and 2.5 times of normal skins, respectively. The expression of these 4 genes was significantly elevated in comparison with normal skins. CONCLUSION: The activation of MEK1/2, ERK1/2 gene expression in hypertrophic scars versus in normal skins might be one of the mechanisms controlling the formation of hypertrophic scars.
Adolescent↗