Proliferation of Luteal Steroidogenic Cells in Cattle

Abstract

The rapid growth of the corpus luteum (CL) after ovulation is believed to be mainly due to an increase in the size of luteal cells (hypertrophy) rather than an increase in their number. However, the relationship between luteal growth and the proliferation of luteal steroidogenic cells (LSCs) is not fully understood. One goal of the present study was to determine whether LSCs proliferate during CL growth. A second goal was to determine whether luteinizing hormone (LH), which is known have roles in the proliferation and differentiation of follicular cells, also affects the proliferation of LSCs. Ki-67 (a cell proliferation marker) was expressed during the early, developing and mid luteal stages and some Ki-67-positive cells co-expressed HSD3B (a steroidogenic marker). DNA content in LSCs isolated from the developing CL increased much more rapidly (indicating rapid growth) than did DNA content in LSCs isolated from the mid CL. The cell cycle-progressive genes CCND2 (cyclin D2) and CCNE1 (cyclin E1) mRNA were expressed more strongly in the small luteal cells than in the large luteal cells. LH decreased the rate of increase of DNA in LSCs isolated from the mid luteal stage but not in LSCs from the developing stage. LH suppressed CCND2 expression in LSCs from the mid luteal stage but not from the developing luteal stage. Furthermore, LH receptor (LHCGR) mRNA expression was higher at the mid luteal stage than at the developing luteal stage. The overall results suggest that the growth of the bovine CL is due to not only hypertrophy of LSCs but also an increase in their number, and that the proliferative ability of luteal steroidogenic cells decreases between the developing and mid luteal stages.

Luteal function during the estrous cycle in arginine-treated ewes fed different planes of nutrition

“…In this and our previous study, cell proliferation in luteal tissues was greatest at the early-, less at the mid-, and least at the late-luteal phase, which corresponds to luteal growth, differentiation and regression respectively (Jablonka-Shariff et al 1993). Similar patterns of change in luteal cell proliferation during the estrous cycle were reported for other species including cows and monkeys (Young et al 2000, Yoshioka et al 2013. In this study, cell proliferation was also affected by plane of nutrition and Arg treatment depending on the stage of estrous cycle.…”

Molecular determinants of a competent bovine corpus luteum: first- vs final-wave dominant follicles

“…Relative to CLs from group A (formed from 'final-wave' DFs), expression of all LHCGR variants was reduced in CLs from group B (derived from first-wave DFs) and was barely detectable in regressing CLs (group C) (Table 5). Based on quantitative measurements of LHCGR expression within the bovine CL during a regular oestrous cycle (Yoshioka et al 2013), we surmise that group B CLs in this study were more similar to regular day 2-3 CLs than day 5-7 CLs. This point is consistent with reduced levels of P4 production by group B relative to group A CLs (Table 3A).…”

Inflammation and angiogenesis in the corpus luteum

“…The corpus luteum (CL) is a transient endocrine structure that secrets progesterone (P4) to establish and maintain intrauterine pregnancy. [1][2][3][4][5] There are two kinds of steroidogenic cells depending on their origin: theca-lutein (small luteal cells) and granulosa-lutein (large luteal cells) cells. 6 In addition to steroidogenic cells, the CL contains endothelial cells (EC), pericytes, fibroblasts and immune cells.…”