关键词: Calcium dynamics round spermatid

Mesh : Animals Calcium / metabolism Homeostasis Lactic Acid / pharmacology Male Models, Biological Rats Rats, Sprague-Dawley Spermatids / drug effects metabolism Thapsigargin / pharmacology

来  源:   DOI:10.1080/19336950.2020.1826787   PDF(Sci-hub)   PDF(Pubmed)

Abstract:
Cytosolic Ca2+ concentration ([Ca2+ ]) has an important role in spermatozoa and hence it regulates fertilization. In male germinal cells, there are indirect evidences that this ion could regulate physiological processes in spermatogenesis. Since little is known about Ca2+ homeostasis in spermatogenic cells, in this work we propose a mathematical model that accounts for experimental [Ca2+ ] dynamics triggered by blockade of the SERCA transport ATPase with thapsigargin in round rat spermatids, without external Ca2+ and with different extracellular lactate concentrations. The model included three homogeneous calcium compartments and Ca2+-ATPase activities sensitive and insensitive to thapsigargin, and it adjusted satisfactorily the experimental calcium dynamic data. Moreover, an extended version of the model satisfactorily adjusted the stationary states of calcium modulated by extracellular lactate, which is consistent with the participation of a low affinity lactate transporter and further lactate metabolism in these cells. Further studies and modeling would be necessary to shed some light into the relation between Ca2+-lactate-ATP homeostasis and cell-cell interactions in the seminiferous tubules that are expected to modulate Ca2+ dynamics by hormonal factors or energetic substrates in meiotic and postmeiotic spermatogenic cells.
摘要:
细胞溶质Ca2浓度([Ca2])在精子中具有重要作用,因此它调节受精。在男性生殖细胞中,有间接证据表明该离子可以调节精子发生的生理过程。由于对生精细胞中的Ca2稳态知之甚少,在这项工作中,我们提出了一个数学模型,该模型解释了圆形大鼠精子细胞中SERCA转运ATPase与thapsigargin阻断所触发的实验[Ca2]动力学,没有外部Ca2+和不同的细胞外乳酸浓度。该模型包括三个均质钙室和Ca2-ATPase活性对thapsigargin敏感和不敏感,并令人满意地调整了实验钙的动态数据。此外,模型的扩展版本令人满意地调整了由细胞外乳酸调节的钙的稳态,这与低亲和力乳酸转运蛋白的参与以及这些细胞中乳酸的进一步代谢是一致的。有必要进行进一步的研究和建模,以阐明生精小管中Ca2-乳酸-ATP稳态与细胞间相互作用之间的关系,这些相互作用有望通过减数分裂和减数分裂后生精细胞中的激素因素或高能底物调节Ca2动力学。
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