Differential localization of α’ and β subunits of protein kinase CK2 during rat spermatogenesis

Alvarado-Díaz, Carlos Patricio; Tapia, Julio C.; Antonelli, Marcelo; Moreno, Ricardo D.

doi:10.1007/s00441-009-0847-1

Cited by 9 publications

(6 citation statements)

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“…These findings are consistent with previous reports that CK2β protein is abundantly and broadly expressed in early spermatogenesis as shown by in situ hybridization and immunohistochemistry in mice. 34,35 However, our results are inconsistent with researches on rats, 43 which indicates that CK2β protein is located in both germ cells and Sertoli cells. This discrepancy may be caused by variations between species.…”

Section: Discussioncontrasting

confidence: 99%

Deletion of Ck2β gene causes germ cell development arrest and azoospermia in male mice

et al. 2019

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Objectives:In humans, non-obstructive azoospermia (NOA) is a major cause of male infertility. However, the aetiology of NOA is largely unknown. Previous studies reported that protein CK2β was abundantly and broadly expressed in spermatogenic cells. Here, we investigate whether protein CK2β participates in spermatogenesis. Materials and Methods: In this study, we separated spermatogenic cells using STA-PUT velocity sedimentation, analysed the expression pattern of protein CK2β by immunoblotting, specifically deleted Ck2β gene in early-stage spermatogenic cells by crossing Ck2β fl mice with Stra8-Cre + mice and validated the knockout efficiency by quantitative RT-PCR and immunoblotting. The phenotypes of Ck2β fl/Δ ;SCre + mice were studied by immunohistochemistry and immunofluorescence. The molecular mechanisms of male germ cell development arrest were elucidated by immunoblotting and TUNEL assay. Results: Ablation of Ck2β gene triggered excessive germ cell apoptosis, germ cell development arrest, azoospermia and male infertility. Inactivation of Ck2β gene caused distinctly reduced expression of Ck2α′ gene and CK2α′ protein.Conclusions: Ck2β is a vital gene for germ cell survival and male fertility in mice.

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Section: Discussioncontrasting

confidence: 99%

Deletion of Ck2β gene causes germ cell development arrest and azoospermia in male mice

et al. 2019

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“…CK2α and CK2α′ expressions were detected in the amnion and choriodecidua at the three trimesters. This result was unexpected because the CK2α′ isoform was found predominantly in the brain and testis, unlike the CK2α isoform, which had low cell and organ specificities [ 28 ]. We found that the expression levels of the CK2 subunits were independent of the FM layers and labor conditions.…”

Section: Discussionmentioning

confidence: 99%

Characterization of RAGE and CK2 Expressions in Human Fetal Membranes

Coste

Bruet

Chollat-Namy

et al. 2023

IJMS

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At the feto-maternal interface, fetal membranes (FM) play a crucial role throughout pregnancy. FM rupture at term implicates different sterile inflammation mechanisms including pathways activated by the transmembrane glycoprotein receptor for advanced glycation end-products (RAGE) belonging to the immunoglobulin superfamily. As the protein kinase CK2 is also implicated in the inflammation process, we aimed to characterize the expressions of RAGE and the protein kinase CK2 as a candidate regulator of RAGE expression. The amnion and choriodecidua were collected from FM explants and/or primary amniotic epithelial cells throughout pregnancy and at term in spontaneous labor (TIL) or term without labor (TNL). The mRNA and protein expressions of RAGE and the CK2α, CK2α′, and CK2β subunits were investigated using reverse transcription quantitative polymerase chain reaction and Western blot assays. Their cellular localizations were determined with microscopic analyses, and the CK2 activity level was measured. RAGE and the CK2α, CK2α′, and CK2β subunits were expressed in both FM layers throughout pregnancy. At term, RAGE was overexpressed in the amnion from the TNL samples, whereas the CK2 subunits were expressed at the same level in the different groups (amnion/choriodecidua/amniocytes, TIL/TNL), without modification of the CK2 activity level and immunolocalization. This work paves the way for future experiments regarding the regulation of RAGE expression by CK2 phosphorylation.

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“…Genetic disruption of CK2 α ′ resulted in a change in the shape of the sperm head in mice during spermatogenesis and in male infertility (Xu et al , ; Escalier et al , ). Recently, it has been reported that the CK2 α ′ subunit showed differential localization during spermatogenesis and CK2 had a possible role at various stages, a process that involved proliferation, meiosis, apoptosis and differentiation (Alvarado‐Díaz et al , ). These reports suggest that CK2 activity or a CK2‐dependent pathway contributes to male infertility.…”

Section: Introductionmentioning

confidence: 99%

Toxicological effect of emodin in mouse testicular gene expression profile

Oshida

Hirakata

Maeda

et al. 2011

J of Applied Toxicology

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Emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) is a herbal medicine extracted from the rhizomes of Rheum palmatum, and is known as an inhibitor of casein kinase II (CK2). The CK2α' knockout mice are known to be male-infertile; however, there have been no reports on the toxicity of emodin in male reproductive organs/tissues. To evaluate the toxicological effects of emodin on differential gene expression profiles of the testis as compared with acrylamide, mice were orally administered emodin and acrylamide for 5 days at a dose of 1000 and 50 mg kg(-1) per day, respectively, and euthanized 24 h after the final administration. Both chemicals induced hypospermatogenesis, eosinophilic change and apoptosis of germ cell. A DNA microarray analysis showed that the IGF-1 receptor signaling was most closely related to the above testicular toxicity induced by emodin, and the RhoA regulation, TGF/WNT and cytoskeletal remodeling, TNFR1 signaling and adenosine A2A receptor signaling were commonly associated with the two chemicals. We selected 36 genes associated with CK2, apoptosis and spermatogenesis and determined their expression by quantitative reverse transcription-polymerase chain reaction (qPCR). Both chemicals perturbed the expression of genes associated with CK2. Genes related to spermatogenesis were also affected, as evidenced by hypospermatogenesis, and eosinophilic change and apoptosis of germ cell. The results suggest that emodin causes testicular toxicity, including apoptosis with related the IGF-1 receptor signaling pathway, and the two chemicals commonly affect CK2, spermatogenesis and sperm motility via four pathways, such as TNFR1 signaling.

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Differential localization of α’ and β subunits of protein kinase CK2 during rat spermatogenesis

Cited by 9 publications

References 50 publications

Deletion of Ck2β gene causes germ cell development arrest and azoospermia in male mice

Deletion of Ck2β gene causes germ cell development arrest and azoospermia in male mice

Characterization of RAGE and CK2 Expressions in Human Fetal Membranes

Toxicological effect of emodin in mouse testicular gene expression profile

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