Abstract
Heat stress negatively affects reproduction in cattle by disrupting the normal function of ovarian granulosa cells (GCs), ultimately leading to oxidative damage and cell death via apoptosis. Heme oxygenase-1(HO-1) is a member of the heat shock protein family, which are associated with cellular antioxidant defenses and anti-apoptotic functions. Recent studies demonstrated that HO-1 is upregulated in heat-stressed cells. In the present study, we investigated the expression of HO-1 in bovine GCs transiently exposed to heat stress and characterized the expression and activity of key oxidative stress enzymes and molecules. We show that heat stress induced oxidative stress and apoptosis, and enhanced Nrf2 and HO-1 expression in primary GC cultures. Knocking down HO-1 expression using siRNA exacerbated both oxidative stress and apoptosis, whereas pre-treating GCs with hemin, which induces HO-1 expression, partially prevented these effects. These findings demonstrate that HO-1 attenuates heat stress-induced apoptosis in bovine GCs by decreasing production of reactive oxygen species and activating the antioxidant response.
Highlights
High ambient temperature is considered to be a critical factor contributing to reduced fertility in cattle in tropical and subtropical countries, the involvement of heat stress in this phenomenon is well documented even in regions with temperate climates [1,2,3]
We show that heat stress induced oxidative stress and apoptosis, and enhanced nuclear factor erythroid 2related factor 2 (Nrf2) and HO‐1 expression in primary granulosa cells (GCs) cultures
Knocking down HO‐1 expression using siRNA exacerbated both oxidative stress and apoptosis, whereas pre‐treating GCs with hemin, which induces HO‐1 expression, partially prevented these effects. These findings demonstrate that HO‐1 attenuates heat stress‐induced apoptosis in bovine GCs by decreasing production of reactive oxygen species and activating the antioxidant response
Summary
High ambient temperature is considered to be a critical factor contributing to reduced fertility in cattle in tropical and subtropical countries, the involvement of heat stress in this phenomenon is well documented even in regions with temperate climates [1,2,3]. Heat stress influences ovarian function, estrous expression, oocyte health, and embryonic development [4, 5]. Normal proliferation and differentiation of GCs are crucial for optimal follicular growth, oocyte development, ovulation, and luteinization [8, 9]. Several studies reported that heat stress adversely affects ovarian GCs, by inducing oxidative damage, endoplasmic reticulum stress, and apoptosis [10,11,12]. Oxidative stress results from imbalances between the generation and elimination of reactive oxygen species (ROS) within cells; excessive ROS generation can overload cellular antioxidant defenses and damage lipids, proteins and DNA, thereby disrupting normal cell function and causing cell death via apoptosis or necrosis [13]. ROS generation and oxidative stress are critically involved in heat stress-induced apoptosis [14, 15]. Recent studies have addressed the molecular mechanisms responsible for the cytoprotective effects of HO-1 against apoptosis, and have suggested its potential relevance as a drug target in anti-oxidative therapies [21, 22]
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