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Epithelial Regeneration (epithelial + regeneration)
Selected AbstractsAdhesion molecules in endometrial epithelium: tissue integrity and embryo implantationJOURNAL OF ANATOMY, Issue 1 2009Harmeet Singh Abstract Cell adhesion in endometrial epithelium is regulated to maintain the continuity and protectiveness of the luminal covering cell layer while permitting interstitial implantation of the embryo during a restricted period of about 4 days. Many apparently normal embryos fail to implant, and epithelial-embryo adhesion remains a poorly understood phenomenon. After menstruation, epithelial regeneration occurs by epiboly from the basal residues of glands, an activity that requires migration on extracellular matrix as well as cell,cell cohesion. Here we review current knowledge of adhesion molecules in the epithelium. [source] Osteopontin as two-sided mediator of intestinal inflammationJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 6 2009Katja Heilmann Abstract Osteopontin (OPN) is characterized as a major amplifier of Th1-immune responses. However, its role in intestinal inflammation is currently unknown. We found considerably raised OPN levels in blood of wild-type (WT) mice with dextran sodium sulfate (DSS)-induced colitis. To identify the role of this mediator in intestinal inflammation, we analysed experimental colitis in OPN-deficient (OPN,/,) mice. In the acute phase of colitis these mice showed more extensive colonic ulcerations and mucosal destruction than WT mice, which was abrogated by application of soluble OPN. Within the OPN,/, mice, infiltrating macrophages were not activated and showed impaired phagocytosis. Reduced mRNA expression of interleukin (IL)-1 , and matrix metalloproteinases was found in acute colitis of OPN,/, mice. This was associated with decreased blood levels of IL-22, a Th17 cytokine that may mediate epithelial regeneration. However, OPN,/, mice showed increased serum levels of tumour necrosis factor (TNF)-,, which could be due to systemically present lipopolysaccharide translocated to the gut. In contrast to acute colitis, during chronic DSS-colitis, which is driven by a Th1 response of the lamina propria infiltrates, OPN,/, mice were protected from mucosal inflammation and demonstrated lower serum levels of IL-12 than WT mice. Furthermore, neutralization of OPN in WT mice abrogated colitis. Lastly, we demonstrate that in patients with active Crohn's disease OPN serum concentration correlated significantly with disease activity. Taken together, we postulate a dual function of OPN in intestinal inflammation: During acute inflammation OPN seems to activate innate immunity, reduces tissue damage and initiates mucosal repair whereas during chronic inflammation it promotes the Th1 response and strengthens inflammation. [source] Influences of Helicobacter pylori on gastric angiogenesis and ulcer healing in miceJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2002Edhi Gunawan Abstract Background and Aims:Helicobacter pylori infection is associated with peptic ulcers; however, it is unclear whether the bacterium delays ulcer healing. We investigated the influence of H. pylori on ulcer healing in mice. We also examined the influence of H. pylori infection on angiogenesis. Methods: An acetic acid ulcer was made in male BALB/c mice. Three days later (day 0), the animals were inoculated with H. pylori SS1 strain. The healing process of the ulcer was examined macroscopically and microscopically on days 0, 6 and 9. The index of angiogenesis was also determined using carmine dye injection. Results: On day 0, angiogenesis began at the ulcer margin while the mucosal epithelia had not yet regenerated. On days 6 and 9, angiogenesis and epithelial regeneration developed and ulcer size reduced. These phenomena were significantly suppressed in mice infected with H. pylori. Conclusion:Helicobacter pylori infection significantly suppressed angiogenesis and delayed ulcer healing. These results indicate that H. pylori plays an important role in ulcer healing. © 2002 Blackwell Publishing Asia Pty Ltd [source] Airway Epithelial Cell Senescence in the Lung AllograftAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2008S. M. Parker Chronic lung allograft dysfunction, manifesting as bronchiolitis obliterans syndrome (BOS), is characterized by airway epithelial injury, impaired epithelial regeneration and subsequent airway remodeling. Increased cellular senescence has been reported in renal and liver allografts affected by chronic allograft dysfunction but the significance of cellular senescence in the airway epithelium of the transplanted lung is unknown. Thirty-four lung transplant recipients, 20 with stable graft function and 14 with BOS, underwent transbronchial lung biopsy and histochemical studies for senescence markers in small airways. Compared to nontransplant control lung tissue (n = 9), lung allografts demonstrate significantly increased airway epithelial staining for senescence-associated beta galactosidase (SA ,-gal) (p = 0.0215), p16ink4a (p = 0.0002) and p21waf1/cip (p = 0.0138) but there was no difference in expression of these markers between stable and BOS affected recipients (p > 0.05). This preliminary cross-sectional study demonstrates that cellular senescence occurs with increased frequency in the airway epithelium of the lung allograft but does not establish any association between airway epithelial senescence and BOS. A prospective longitudinal study is required to better address any potential causal association between airway epithelial senescence in stable allograft recipients and the subsequent development of BOS. [source] Erythropoietin administration protects against functional impairment and cell death after ischaemic renal injury in pigsBJU INTERNATIONAL, Issue 1 2007COLIN J. FORMAN OBJECTIVE To determine whether the administration of erythropoietin at the time of ischaemic renal injury (IRI) inhibits apoptosis, enhances tubular epithelial regeneration and promotes renal functional recovery, as it does in rodent models, in a higher mammalian model. MATERIALS AND METHODS The model of IRI involved unilateral nephrectomy in pigs, followed a week later by renal artery occlusion for 1 h, followed by reperfusion for 5 days. Pigs were randomized to receive erythropoietin 5000 units/kg intravenously at the time of ischaemia, followed by 1000 units/kg subcutaneously daily, or no treatment (six pigs each). Renal function and structure were analysed; blood and urine were collected daily to determine serum creatinine level, blood urea nitrogen, and creatinine clearance. Animals were killed after 5 days to obtain the injured kidneys. The kidneys were examined histologically for evidence of cellular mitosis, apoptosis and necrosis. RESULTS Erythropoietin significantly abrogated renal dysfunction after IRI compared with controls at 12 h after injury; the mean (sem) creatinine clearance (as a percentage of baseline) for IRI was 68.2 (6)% vs erythropoietin-IRI 94.9 (8.9)% (P = 0.027), although by 36 h this was no longer significant, with values of 73.8 (12.7)% vs 95.9 (12)%, respectively (P = 0.23). Erythropoietin also significantly reduced the amount of cell death on histological analysis after 5 days of reperfusion, with a median (range) for IRI of 5.5 (1,45) vs erythropoietin-IRI of 1.5 (0,4) (P = 0.043). CONCLUSION This study confirms the potential clinical applications of erythropoietin as a novel therapeutic agent in patients at risk of IRI. [source] Expression and role of Notch signalling in the regeneration of rat tracheal epitheliumCELL PROLIFERATION, Issue 1 2009X.-B. Ma Objectives:, This study is to explore the role of Notch signalling during the regeneration of rat tracheal epithelium after injury induced by 5-fluorouracil (5-FU). Materials and methods:, We developed an ex vivo model of rat tracheal epithelial regeneration using 5-FU to induce injury. Expression levels of members of the Notch signalling pathway, ABCG2, CK19, and proliferating cell nuclear antigen (PCNA) were examined by reverse transcription,polymerase chain reaction, Western blot, and immunofluorescence. One group of tracheas were cultured in the medium with a ,-secretase inhibitor or Jag-1 peptide after 5-FU treatment and another group were pre-treated with the ,-secretase inhibitor or Jag-1 peptide before 5-FU treatment. The expression changes of ABCG2, CK19, and PCNA were examined by Western blot or immunofluorescence and the morphologic changes were observed by haematoxylin and eosin stain during the recovery process. Results:, Expression levels of Notch3, Jagged1, and Hey1 were increased in rat tracheal epithelial cells after treatment with 5-FU. During injury recovery, disruption of Notch signalling by treatment with the ,-secretase inhibitor reduced expression of ABCG2 and PCNA, but promoted expression of CK19, while persistent activation of Notch signalling promoted expression of ABCG2 and PCNA, but reduced expression of CK19. Under both conditions, recovery from injury was reduced. However, blocking Notch signalling prior to 5-FU treatment led to the complete blockage of recovery, while activating Notch signalling before 5-FU treatment promoted recovery. Conclusions:, During tracheal epithelial regeneration, Notch signalling maintains an undifferentiated state and promotes proliferation among a population of tracheal epithelial cells. [source] 4242: Elschnig pearl formation and disappearanceACTA OPHTHALMOLOGICA, Issue 2010N HIRNSCHALL Purpose To observe and analyze morphological changes of Elschnig pearls in eyes with after-cataract. Methods Pseudophakic eyes with pronounced regeneratory posterior capsule opacification were included in the prospective studies. In the first study the natural course of Elschnig pearls was observed during days and weeks. In the second study morphological changes immediately after a Nd:YAG-capsulotomy were observed. And in two further studies the Nd:YAG laser capsulotomy was modified and the effect on Elschnig pearls was observed. Results In the first study, in total 6309 Elschnig pearls (85 eyes) were analyzed. On average, four pearls were found per square millimeter (range, 0.2-9.7/mm2) with a mean cumulative area of 0.66 mm2) (range, 0.03-2.18 mm2) of all marked pearls per eye and follow-up. The mean pearl size was 9630 microm2 (range, 2390-33,745 microm2) at baseline. The mean change of a pearl per day was 583 microm2 (range, 175-1631 microm2) or a 6% change in area. In the second study in total, 2431 Elschnig pearls (20eyes) were observed. Of these, 535 pearls (30.6%) disappeared, and 503 pearls (27.6%) survived on the remaining capsule peripheral to the capsulotomy opening. Conclusion Elschnig pearls disappear and appear within days. The degree of progression and regression varies greatly between eyes. Capsulotomy had an immediate impact on the morphology of PCO outside the capsulotomy opening. Knowledge about Elschnig pearl turnover may be of importance for attempts to modulate lens epithelial regeneration or lens regrowth and for lens-refilling procedures. [source] | |||||||||||||