Abstract
The aim of the present study was to evaluate the expression and effect of rat mitofusin-2 (rMfn2) in the ovaries and other organs in rats. Rat models were developed by the intraovarian microinjection of an rMfn2-overexpressing lentiviral vector. Lenti-green fluorescent protein (GFP)-rMfn2 was microinjected into rat ovaries at a dosage of 2×106 tuberculin units virosome (n=25) and lenti-GFP was microinjected as a control (n=25). The expression of rMfn2 in the ovaries and other tissues was observed by fluorescence microscopy on days 7, 15, 30, 45 and 60 after the microinjection (n=5/day from each group). The serum levels of estradiol (E2), progesterone (P), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were determined by radioimmunoassay. Western blotting was used for the quantitative analysis of the expression of rMfn2 and the progesterone receptor (PR), estradiol receptor (ER), luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR). The expression of rMfn2 was detected on day 7 after infection, increased with time and was maintained efficiently until day 60. In addition, rMfn2 was highly expressed in the fallopian tubes, uterus, cardiac muscle, liver and kidney, but expressed at a low level in adipose tissue. The serum levels of E2 and P in the model group were significantly increased compared with those in the control group, whereas the FSH and LH levels showed no significant difference between groups. The expression levels of the ER and PR in the model group were higher than those in the control group; however, no significant difference was observed between groups for the expression levels of LHR and FSHR. These findings suggest that the intraovarian microinjection of lenti-GFP-rMfn2 resulted in a significant time-dependent overexpression of rMfn2 in various organs, and that rMfn2 overexpression in rat ovaries changed the endocrine function and promoted follicular development.
Highlights
Mitofusin‐2 (Mfn2), named hyperplasia suppressor gene (HSG), is a transmembrane GTPase embedded in the mitochondrial outer membrane that mediates mitochondrial fusion [1]
Rat models were developed through the intraovarian microinjection of an rat mitofusin‐2 (rMfn2)‐overexpressing lentiviral vector in order to detect the effect and expression profile of rMfn2 in rats
It was observed that even though the lentiviral vector was microinjected into the sub‐envelope of the ovary, the fluorescence density in the ovary was enhanced with the prolongation of time and an efficient and strong expression was maintained until day 60 after infection
Summary
Mitofusin‐2 (Mfn2), named hyperplasia suppressor gene (HSG), is a transmembrane GTPase embedded in the mitochondrial outer membrane that mediates mitochondrial fusion [1]. Mfn deficiency and mutations have been linked to human neurodegenerative diseases, including Charcot‐Marie‐Tooth type 2A and other hereditary motor and sensory neuropathies [2,3,4]. A number of studies have shown that Mfn regulates both mitochondrial fusion and mitochondrial apoptotic signaling and is involved in the pathogenesis of disease conditions such as obesity, type 2 diabetes, insulin resistance and the survival of different epithelial cancer cell lines [5,6,7,8,9,10,11]. A further study has shown that the overexpression of Mfn inhibits hepatocellular carcinoma cell proliferation and induces apoptosis via Bax, and adenovirus‐mediated Mfn upregulation significantly suppresses the growth of subcutaneous tumors in nude mice both in vivo and in vitro [14]. There are a large number of studies about Mfn, but few of these are morphological studies
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