Pelvic organ prolapse (POP) is the descent of the pelvic organs,including bladder, uterus, vagina and rectum, resulting in pelvic discomfort, urinary and fecal incontinence and sexual dysfunction(1)The prevalence of s...Pelvic organ prolapse (POP) is the descent of the pelvic organs,including bladder, uterus, vagina and rectum, resulting in pelvic discomfort, urinary and fecal incontinence and sexual dysfunction(1)The prevalence of symptomatic POP in China is 9.56%according to a cross-sectional study involving 54,000 adult women in six provinces in the mainland of China (unpublished data). The etiology of this disorder is multifactorial, including race, age, body mass index(BMI), parity and menopause (1)The loss of the integrity of vaginal connective tissue has been demonstrated to weaken the pelvic floor support and promote the development of POP.展开更多
Purpose： Microgravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgra...Purpose： Microgravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgravity （SMG）. Methods： We utilized the rotary cell culture system （RCCS-1） to explore the subsequent effects of SMG on human umbilical vein endothelial cells （HUVECs）. Results： SMG-treated HUVECs appeared obvious growth inhibition after return to normal gravity, which might be attributed to a set of responses including alteration of cytoskeleton, decreased cell adhesion capacity and increased apoptosis. Expression levels of mTOR and its downstream Apaf-1 were increased during subsequent culturing after SMG. miR-22 was up-regulated and its target genes SRF and LAMC1 were down-regulated at mRNA levels. LAMC1 siRNAs reduced cell adhesion rate and inhibited stress fiber formation while SRF siRNAs caused apoptosis. Conclusion： SMG has the subsequent biological effects on HUVECs, resulting in growth inhibition through mTOR signaling and miR-22-mediated mechanism.展开更多
基金supported by the Chinese Academy of Medical Sciences Initiative for Innovative Medicine (CAMS-2017-I2M-1002)
文摘Pelvic organ prolapse (POP) is the descent of the pelvic organs,including bladder, uterus, vagina and rectum, resulting in pelvic discomfort, urinary and fecal incontinence and sexual dysfunction(1)The prevalence of symptomatic POP in China is 9.56%according to a cross-sectional study involving 54,000 adult women in six provinces in the mainland of China (unpublished data). The etiology of this disorder is multifactorial, including race, age, body mass index(BMI), parity and menopause (1)The loss of the integrity of vaginal connective tissue has been demonstrated to weaken the pelvic floor support and promote the development of POP.
基金This study was supported by the ＂National Natural Science Foundation of China （No, 31270903）＂ and the Fundamental Research Funds for the Central Universities （3132016330）,
文摘Purpose： Microgravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgravity （SMG）. Methods： We utilized the rotary cell culture system （RCCS-1） to explore the subsequent effects of SMG on human umbilical vein endothelial cells （HUVECs）. Results： SMG-treated HUVECs appeared obvious growth inhibition after return to normal gravity, which might be attributed to a set of responses including alteration of cytoskeleton, decreased cell adhesion capacity and increased apoptosis. Expression levels of mTOR and its downstream Apaf-1 were increased during subsequent culturing after SMG. miR-22 was up-regulated and its target genes SRF and LAMC1 were down-regulated at mRNA levels. LAMC1 siRNAs reduced cell adhesion rate and inhibited stress fiber formation while SRF siRNAs caused apoptosis. Conclusion： SMG has the subsequent biological effects on HUVECs, resulting in growth inhibition through mTOR signaling and miR-22-mediated mechanism.
