Hepatocyte growth factor induces rat ovarian surface epithelial cell mitosis or apoptosis depending on the presence or absence of an extracellular matrix.
Abstract: The present studies showed that sequential treatment with equine CG (eCG) and hCG not only induced an increase in ovarian weight, but also caused an estimated 4.6-fold increase in the number of ovarian surface epithelial cells. In addition, eCG-hCG treatment increased ovarian hepatocyte growth factor (HGF) messenger RNA levels. These studies also demonstrated that rat primary ovarian surface epithelial cells as well as a cell line derived from rat ovarian surface epithelium (i.e. ROSE-179 cells) do not express the LH (hCG) receptor. Both of these cells express c-Met, the receptor for HGF. To assess the effects of hCG and HGF on ovarian surface epithelial cell mitosis, ROSE-179 cells were cultured for 24 h in serum-supplemented medium on either glass or the synthetic fibronectin-like extracellular matrix protein, pronectin (RGD). The cells were then cultured for 24 h in serum-free medium in the presence or absence of hCG or HGF. The numbers of cells at 2, 24, and 48 h of culture were determined. The percentage of apoptotic cells was assessed by in situ DNA staining at 48 h of culture. In the serum-supplemented medium in the presence or absence of RGD, the number of ROSE-179 cells doubled. In serum-free medium, cell proliferation was reduced, and the percentage of apoptotic nuclei ranged between 10-15% regardless of the substrate. Neither mitosis nor apoptosis was influenced by hCG in the presence or absence of RGD. For ROSE-179 cells cultured in serum-free medium on RGD, HGF induced mitosis, resulting in a 2.8 +/- 0.2-fold increase in cell number compared with the 24 h control values. On a glass substrate in serum-free medium, HGF did not induce mitosis, but increased the percentage of apoptotic nuclei. Time-lapse photographic analysis revealed that on RGD, cells undergoing HGF-induced mitosis showed a transient reduction in cell contact. On glass, HGF caused many cells to completely lose contact and separate from each other. Collectively, these data suggest that in vivo gonadotropins stimulate HGF expression and ovarian surface epithelial cell proliferation. Based on in vitro studies, it is likely that the mitogenic action of hCG is mediated by HGF. However, HGF only induces mitosis in the presence of an extracellular matrix.
Publication Date: 1999-05-26 PubMed ID: 10342884DOI: 10.1210/endo.140.6.6773Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- P.H.S.
Summary
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The research article investigates how the hepatocyte growth factor influences the process of cell mitosis or apoptosis in rat ovarian surface epithelial cells, depending on the presence or absence of an extracellular matrix. The study finds that gonadotropins stimulate the expression of HGF which promotes the proliferation of ovarian surface epithelial cells, but HGF only induces mitosis when an extracellular matrix is present.
Experimental Process
- The study subjects were rat ovarian surface epithelial cells and a related cell line known as ROSE-179 cells.
- Both sets of cells were found to express c-Met, the receptor for Hepatocyte Growth Factor (HGF), but they did not express the LH (HCG) receptor.
- The ROSE-179 cells were cultured for 24 hours in serum-supplemented medium on either glass or a synthetic fibronectin-like extracellular matrix protein, pronectin (RGD).
- The cells were further cultured in serum-free medium in the presence or absence of hCG or HGF.
- The number of cells and the percentage of apoptotic cells were determined at different intervals of time.
Key Findings
- The presence or absence of the synthetic fibronectin-like extracellular matrix protein, pronectin (RGD), had significant effects on the reaction of the cells to HGF. The number of ROSE-179 cells doubled in serum-supplemented medium with or without RGD.
- In serum-free medium, HGF induced mitosis (cell division) among the cells cultured on RGD, resulting in a marked increase in cell numbers. However, on a glass substrate in serum-free medium, HGF did not induce mitosis, but instead increased the percentage of apoptotic cells (cells undergoing programmed cell death).
- Cell proliferation was reduced in the serum-free medium and the percentage of apoptotic nuclei ranged between 10-15% regardless of the substrate.
Conclusion
- The study concludes that gonadotropins in vivo stimulate the Hepatocyte Growth Factor (HGF) expression and ovarian surface epithelial cell proliferation. However, the HGF only induces mitosis (cell division) in the presence of an extracellular matrix.
- The findings suggest that HGF may have potential use in the manipulation of cell proliferation in ovarian applications, but consideration must be given to the environment in which the cells are present and whether there is an extracellular matrix.
Cite This Article
APA
Hess S, Gulati R, Peluso JJ.
(1999).
Hepatocyte growth factor induces rat ovarian surface epithelial cell mitosis or apoptosis depending on the presence or absence of an extracellular matrix.
Endocrinology, 140(6), 2908-2916.
https://doi.org/10.1210/endo.140.6.6773 Publication
Researcher Affiliations
- Department of Obstetrics and Gynecology, University of Connecticut Health Center, Farmington, USA.
MeSH Terms
- Animals
- Apoptosis / drug effects
- Cell Communication / drug effects
- Cell Movement / drug effects
- Chorionic Gonadotropin / pharmacology
- Epithelial Cells / drug effects
- Extracellular Matrix / physiology
- Female
- Gonadotropins / pharmacology
- Hepatocyte Growth Factor / genetics
- Hepatocyte Growth Factor / pharmacology
- Mitosis / drug effects
- Oligopeptides / metabolism
- Ovary / cytology
- Ovary / drug effects
- Proto-Oncogene Proteins c-met / analysis
- RNA, Messenger / analysis
- Rats
- Rats, Wistar
- Receptors, LH / analysis
Grant Funding
- 1-RO-1-HD-33467-01A / NICHD NIH HHS
Citations
This article has been cited 7 times.- Al-Amri IS, Kadim IT, Al-Kindi AA, Khalaf SK, Al-Harrasi AS, Al-Hashmi SA, Al-Shibli AA, Al-Hadi WM, Al-Mahimuli MK, Jamshidi-Adegani F, Vakilian S, Al-Amri AI, Al-Yaqoobi SS, Al-Riyami KO. Microscopic Evaluation of Ovarian Surface Epithelium Following Treatment with Conjugated Estrogens in a Mouse Model.. Asian Pac J Cancer Prev 2022 Jun 1;23(6):1913-1920.
- Kwon Y, Godwin AK. Regulation of HGF and c-MET Interaction in Normal Ovary and Ovarian Cancer.. Reprod Sci 2017 Apr;24(4):494-501.
- Ng A, Barker N. Ovary and fimbrial stem cells: biology, niche and cancer origins.. Nat Rev Mol Cell Biol 2015 Oct;16(10):625-38.
- Chakravarti B, Dwivedi SK, Mithal A, Chattopadhyay N. Calcium-sensing receptor in cancer: good cop or bad cop?. Endocrine 2009 Jun;35(3):271-84.
- Perniconi SE, Simões Mde J, Simões Rdos S, Haidar MA, Baracat EC, Soares JM Jr. Proliferation of the superficial epithelium of ovaries in senile female rats following oral administration of conjugated equine estrogens.. Clinics (Sao Paulo) 2008 Jun;63(3):381-8.
- Xie Q, Liu KD, Hu MY, Zhou K. SF/HGF-c-Met autocrine and paracrine promote metastasis of hepatocellular carcinoma.. World J Gastroenterol 2001 Dec;7(6):816-20.
- Lail-Trecker MR, Peluso CE, Peluso JJ. Hepatocyte growth factor disrupts cell contact and stimulates an increase in type 3 inositol triphosphate receptor expression, intracellular calcium levels, and apoptosis of rat ovarian surface epithelial cells.. Endocrine 2000 Jun;12(3):303-14.
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