Cellular and functional adaptation to thermal stress in ovarian granulosa cells in mammals

J Therm Biol. 2020 Aug:92:102688. doi: 10.1016/j.jtherbio.2020.102688. Epub 2020 Aug 12.

Abstract

Climate change represents a significant environmental challenge to human welfare. One of many negative impacts may be on animal reproduction. Elevated ambient temperature unfavourably influences reproductive processes in mammals. High temperature can affect reproductive processes such as follicle development and may alter follicular fluid concentrations of amino acids, fatty acids, minerals, enzymes, antioxidants defence and growth factors. These impacts may lead to inferior oocyte competence and abnormal granulosa cell (GCs) function. Mammalian oocytes are enclosed by GCs that secret hormones and signalling molecules to promote oocyte competence. GCs are essential for proper follicular development, oocyte maturation, ovulation, and luteinization. Many environmental stressors, including thermal stress, affect GC function and alter oocyte development and growth. Several studies documented a link between elevated ambient temperature and increased generation of cellular reactive oxygen species (ROS). ROS can damage DNA, reduce cell proliferation, and induce apoptosis in GCs, thus altering oocyte development. Additionally, thermal stress induces upregulation of thermal shock proteins, such as HSP70 and HSP90. This review provides an update on the influence of thermal stress on GCs of mammals. Discussions include impacts to steroidogenesis (estradiol and progesterone), proliferation and cell cycle transition, apoptosis, oxidative stress (ROS), antioxidants related genes, heat shock proteins (HSPs) and endoplasmic reticulum responses.

Keywords: Apoptosis; Granulosa cells (GCs); Oxidative stress; Steroidogenesis hormones; Thermal stress.

Publication types

  • Review

MeSH terms

  • Adaptation, Physiological
  • Animals
  • Apoptosis
  • Cell Proliferation
  • Female
  • Granulosa Cells / cytology
  • Granulosa Cells / metabolism*
  • Heat-Shock Proteins / metabolism
  • Heat-Shock Response*
  • Humans
  • Oocytes / cytology
  • Oocytes / growth & development
  • Ovary / cytology*
  • Ovary / physiology
  • Oxidative Stress
  • Reproduction

Substances

  • Heat-Shock Proteins