An immunological approach to study gonadotropin action at the cellular and molecular level

Moudgal, Raghuveer N.; Dighe, Rajan R.

doi:10.1007/bf01119907

Cited by 3 publications

(1 citation statement)

References 37 publications

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“…The major blockade in elucidating these mechanisms is lack of suitable in vitro culture systems. Our group has been employing the strategy of using specific antibodies against gonadotropins to arrest gonadal differentiation in order to identify the LH and FSH dependent functions in the gonads (Shivshanker et al 1977;Murty et al 1979;Moudgal and Dighe 1985;Vaishnav and Moudgal 1991). In the present study, an attempt has been made to study the role of gonadotropins in spermatogonial proliferation by employing gonadotropin antibodies.…”

Section: Introductionmentioning

confidence: 99%

Pituitary gonadotropins regulate spermatogonial differentiation and proliferation in the rat‡

et al. 1996

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The relative regulatory roles of the pituitary gonadotropins, luteinizing hormone and follicle stimulating hormone in the spermatogonial proliferation has been studied using specific antibodies against these hormones in the immature rats. Immunoneutralization of luteinizing hormone for 7 days resulted in significant reduction in tetraploid cells and total absence of haploid cells, while there was a relative increase in the diploid population. This was also accomopanied by a decrease in spermatogonial proliferation as indicated by a decrease in [ 3 H] thymidine incorporation into DNA by purified spermatogonia. Administration of follicle stimulating hormone a/s for 7 days also caused a significant decrease in the rate of spermatogonial proliferation. Withdrawal of follicle stimulating hormone led to a significant reduction in tetraploid and haploid cells. However interestingly, it failed to totally abolish the appearance of these cells. Administration of testosterone (3 mg/day/rat) for 2 days along with the gonadotropin a/s could partially reverse the effect on spermatogonial proliferation. It is concluded that (i) both luteinizing hormone and follicle stimulating hormone are involved in spermatogonial proliferation, (ii) lack of testosterone consequent of the neutralization of luteinizing hormone prevented the entry of spermatogonial cells into meiosis, (iii) testosterone may be involved in spermatogonia] proliferation providing a mitotic signal and (v) both follicle stimulating hormone and testosterone act synergistically and lack of any one of the hormones results in impairment of spermatogonial proliferation.

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Section: Introductionmentioning

confidence: 99%

Pituitary gonadotropins regulate spermatogonial differentiation and proliferation in the rat‡

et al. 1996

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Relative ability of ovine follicle stimulating hormone and itsβ-subunit to generate antibodies having bioneutralization potential in nonhuman primates

1989

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Selective immunoneutralization of luteinizing hormone results in the apoptotic cell death of pachytene spermatocytes and spermatids in the rat testis

Marathe

Shetty

Dighe

1995

Endocr

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The selective withdrawal of pituitary gonadotropins through specific antibodies is known to cause disruption of spermatogenesis. The cellular mechanism responsible for the degenerative changes under isolated effect of luteinizing hormone (LH) deprivation is not clear. Using antibodies specific to LH we have investigated the effect of immunoneutralization of LH on apoptotic cell death in the testicular cells of the immature and the adult rats. Specific neutralization of LH resulted in apoptotic cell death of germ cells, both in the immature and the adult rats. The germ cells from control animals showed predominantly high molecular weight DNA, while the antiserum treated group showed DNA cleavage into low molecular weight DNA ladder characteristic of apoptosis. This pattern could be observed within 24 h of a/s administration and the effect could be reversed by testosterone. The germ cells were purified by centrifugal elutriation and the vulnerability of germ cell types to undergo apoptosis under LH deprivation was investigated. The round spermatids and the pachytene spermatocytes were found to be the most sensitive germ cells to lack of LH and underwent apoptosis. Interestingly, spermatogonial cells were found to be the least sensitive germ cells to the lack of LH in terms of apoptotic cell death. Results show that LH, in addition to being involved in the germ cell differentiation, is also involved in cell survival and prevent degeneration of germ cells during spermatogenesis. Apoptotic DNA fragmentation may serve as a useful marker for the study of hormonal regulation of spermatogenesis and the specific neutralization of gonadotropic hormones can be a reliable model for the study of the molecular mechanism of apoptosis.

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An immunological approach to study gonadotropin action at the cellular and molecular level

Cited by 3 publications

References 37 publications

Pituitary gonadotropins regulate spermatogonial differentiation and proliferation in the rat‡

Pituitary gonadotropins regulate spermatogonial differentiation and proliferation in the rat‡

Relative ability of ovine follicle stimulating hormone and itsβ-subunit to generate antibodies having bioneutralization potential in nonhuman primates

Selective immunoneutralization of luteinizing hormone results in the apoptotic cell death of pachytene spermatocytes and spermatids in the rat testis

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