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Decreased expression of c-kit and telomerase in a rat model of chronic endometrial ischemia.

Hu J, Yuan R - Med. Sci. Monit. (2011)

Bottom Line: Pou5f1and c-kit mRNA was examined by qPCR.C-kit, caspase3 and telomerase were detected by Western blot.The expression level of caspase3 was significantly higher in the experimental group compared with that in the control group (P<0.05).

View Article: PubMed Central - PubMed

Affiliation: Department of Obstetrics and Gynecology, 1st Affiliated Hospital, Chongqing Medical University, Chongqing, China.

ABSTRACT

Background: It was unclear whether chronic endometrial ischemia contributed to the pathogenesis of thin endometrium and was associated with decreased endometrial stem/progenitor cell. Thus, we explored the role of chronic endometrial ischemia in the pathogenesis of thin endometrium and its effect on endometrial stem/progenitor cells apoptosis.

Material/methods: In vitro, endometrial side population (ESP) cell apoptosis models were built, and apoptosis was quantified by fluorescence-activated cell sorter (FACS) analysis, pou5f1, and c-kit mRNA was detected by qPCR. In vivo, a rat model of chronic endometrial ischemia was induced by performing bilateral uterine artery ligation. TERT and caspase3 were detected by immunohistochemistry. Pou5f1and c-kit mRNA was examined by qPCR. C-kit, caspase3 and telomerase were detected by Western blot.

Results: In the in vitro endometrial SP (ESP) cells apoptosis model, we found that the apoptotic rate was gradually increased with time, prolonging the expression of TERT, and c-kit mRNA was gradually decreased. In the in vivo endometrial SP (ESP) cells apoptosis model, we found that endometrial thickness, luminal epithelium thickness, gland epithelium thickness and the number of glands in the experiment group were significantly decreased compared with those in the control group (P<0.05). The expression levels of c-kit, pou5f1 and telomerase was significantly lower in the experimental group than those in the control group (P<0.05). The expression level of caspase3 was significantly higher in the experimental group compared with that in the control group (P<0.05).

Conclusions: The present work shows that chronic ischemia and chronic endometrial ischemia-associated stem/progenitor cells apoptosis may be responsible for the pathogenesis of thin endometrium.

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Histological examination of the rat endometrium. Hematoxylin and eosin (H-E) staining. (A) Representative endometrium sections of control rats; ×50 magnification. (B) Representative endometrium sections of experimental rats; ×50 magnification. (C) Representative endometrium sections of control rats; ×200 magnification. (D) Representative endometrium sections of experimental rats; ×200 magnification.
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f2-medscimonit-17-4-br103: Histological examination of the rat endometrium. Hematoxylin and eosin (H-E) staining. (A) Representative endometrium sections of control rats; ×50 magnification. (B) Representative endometrium sections of experimental rats; ×50 magnification. (C) Representative endometrium sections of control rats; ×200 magnification. (D) Representative endometrium sections of experimental rats; ×200 magnification.

Mentions: Endometrial thickness (H0), luminal epithelium thickness (H1), gland epithelium thickness (H2) and the number of glands (N) in the experimental group were significantly decreased compared with those in the control group (P<0.05; Figure 2, Table 1).


Decreased expression of c-kit and telomerase in a rat model of chronic endometrial ischemia.

Hu J, Yuan R - Med. Sci. Monit. (2011)

Histological examination of the rat endometrium. Hematoxylin and eosin (H-E) staining. (A) Representative endometrium sections of control rats; ×50 magnification. (B) Representative endometrium sections of experimental rats; ×50 magnification. (C) Representative endometrium sections of control rats; ×200 magnification. (D) Representative endometrium sections of experimental rats; ×200 magnification.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3539516&req=5

f2-medscimonit-17-4-br103: Histological examination of the rat endometrium. Hematoxylin and eosin (H-E) staining. (A) Representative endometrium sections of control rats; ×50 magnification. (B) Representative endometrium sections of experimental rats; ×50 magnification. (C) Representative endometrium sections of control rats; ×200 magnification. (D) Representative endometrium sections of experimental rats; ×200 magnification.
Mentions: Endometrial thickness (H0), luminal epithelium thickness (H1), gland epithelium thickness (H2) and the number of glands (N) in the experimental group were significantly decreased compared with those in the control group (P<0.05; Figure 2, Table 1).

Bottom Line: Pou5f1and c-kit mRNA was examined by qPCR.C-kit, caspase3 and telomerase were detected by Western blot.The expression level of caspase3 was significantly higher in the experimental group compared with that in the control group (P<0.05).

View Article: PubMed Central - PubMed

Affiliation: Department of Obstetrics and Gynecology, 1st Affiliated Hospital, Chongqing Medical University, Chongqing, China.

ABSTRACT

Background: It was unclear whether chronic endometrial ischemia contributed to the pathogenesis of thin endometrium and was associated with decreased endometrial stem/progenitor cell. Thus, we explored the role of chronic endometrial ischemia in the pathogenesis of thin endometrium and its effect on endometrial stem/progenitor cells apoptosis.

Material/methods: In vitro, endometrial side population (ESP) cell apoptosis models were built, and apoptosis was quantified by fluorescence-activated cell sorter (FACS) analysis, pou5f1, and c-kit mRNA was detected by qPCR. In vivo, a rat model of chronic endometrial ischemia was induced by performing bilateral uterine artery ligation. TERT and caspase3 were detected by immunohistochemistry. Pou5f1and c-kit mRNA was examined by qPCR. C-kit, caspase3 and telomerase were detected by Western blot.

Results: In the in vitro endometrial SP (ESP) cells apoptosis model, we found that the apoptotic rate was gradually increased with time, prolonging the expression of TERT, and c-kit mRNA was gradually decreased. In the in vivo endometrial SP (ESP) cells apoptosis model, we found that endometrial thickness, luminal epithelium thickness, gland epithelium thickness and the number of glands in the experiment group were significantly decreased compared with those in the control group (P<0.05). The expression levels of c-kit, pou5f1 and telomerase was significantly lower in the experimental group than those in the control group (P<0.05). The expression level of caspase3 was significantly higher in the experimental group compared with that in the control group (P<0.05).

Conclusions: The present work shows that chronic ischemia and chronic endometrial ischemia-associated stem/progenitor cells apoptosis may be responsible for the pathogenesis of thin endometrium.

Show MeSH
Related in: MedlinePlus