The Mechanism Of Endoplasmic Reticulum Stress Mediated Female Stress Urinary Incontinence

Female stress urinary incontinence (SUI) refers to when the bladderpressure exceeds maximum urethral pressure, detrusor withoutshrinkage leads to can’t control urine, show when exertion, sneezing,coughing, out of the control of urinary leakage phenomenon. Theoccurrence factors mainly related to pregnancy and vaginal delivery,obesity, genetics and age, and so on.Studies pointed out that more than25%of adult women sufferingfrom varying degrees of SUI, of which about half for stress urinaryincontinence. The incidence of this disease of older women can be ashigh as above30%.Its treatment: conservative treatment is feasible intervention lifestyle,behavioral therapy, physical therapy and drug therapy; Surgical repaircan be performed, the structure of the tissue replacement andreconstruction. However, the treatment effect is not ideal enough.In recent years, many researchers to explore its pathogenesis.Found elastin, collagen synthesis to reduce or increase degradation andapoptosis occurs, cause pelvic floor tissues relaxation, neurotransmitter,estrogen receptor has also observed that the quantitative changehappened. But now based in SUI know etiology and molecular mechanism is still poorly understood. According to the literature and ourstudy, senile rats increased endoplasmic reticulum stress level exceptionduring the process of aging, and the occurrence of endoplasmicreticulum stress directly control the protein in the cell such asdegradation of elastin and collagen synthesis, level, therefore,speculated that the occurrence of endoplasmic reticulum stress mayhave an association with the SUI.This research through the collection of patient samples and to makeanimal model, to investigate the relationship between the endoplasmicreticulum stress and SUI, trying to illustrate SUI mechanism, providenew strategy for clinical treatment SUI.The first part of SUI in endoplasmic reticulum stress levels in thepatients group were observedObjective: to observe the SUI patients with pathological changesand endoplasmic reticulum stress related protein expression changes.Methods: for patients with anterior wall vaginal tissue samples, forHE and immunohistochemical staining.Results: the pathologic histology showed smooth muscle cells havedifferent degrees of muscle fiber sparse, interstitial edema; Immuneorganized dyeing results show that, compared with the control group,patients with SUI organization PERK, p-JNK, Ub expression increased,the p-eIF2α, Bip, ATF4, p62expression decreased. Conclusion: SUI continued endoplasmic reticulum stress may havehappened to in the organization, and autophagy activity reduced.The second part, based on SUI rat model the molecular mechanismof this study was to evaluateObjective: from the perspective of endoplasmic reticulum stressexplore the molecular mechanism of SUI.Methods: model rats SUI, anterior wall for rat vagina tissue forwestern blot analysis and gene amplification, observation downstream ofendoplasmic reticulum stress related molecular expression.Results: compared with control group, PERK, p-JNK, CHOP,GADD34, caspase12expression increase in the diseased tissue of SUIrats; p-eIF2α, Bip, Bcl-2and autophagy related protein such as LC3,these expression decline. The change of endoplasmic reticulum stressrelated proteins consistent with diseased tissue in patients, at the sametime proapoptosis protein expression increased obviously.Conclusion: SUI model diseased tissue in a constant ofendoplasmic reticulum stress conditions, the dephosphorylation of eIF2α to make translation recovered, but tend to increase the expression ofproapoptosis protein, rather than the adaptive adjustment, which may bethe molecular basis of cell function lose in the lesion site, and leading toSUI.