Change of Genes in Calcium Transport Channels Caused by Hypoxic Stress in the Placenta, Duodenum, and Kidney of Pregnant Rats1

Yang, Hyun; An, Beum‐Soo; Choi, Kyung‐Chul; Jeung, Eui‐Bae

doi:10.1095/biolreprod.112.103705

Cited by 16 publications

(11 citation statements)

References 81 publications

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“…In another study, NCKX3 was demonstrated to be expressed in the rat duodenum (27). NCKX3 in the basolateral membrane of intestinal tissue transports calcium to the blood, thus it has a key role in calcium absorption (41). Due to this function of NCKX3, abnormal expression of NCKX3 can induce decreased calcium absorption in the duodenum and calcium reabsorption in the kidney; furthermore, it may result in hypocalcemia and osteoporosis (42).…”

Section: Discussionmentioning

confidence: 99%

“…These channels are located in a variety of organs and have the ability to function at metabolically appropriate times (39). A number of previous studies have reported on the expression and regulation of various cation channel proteins; however, there are no similar reports for such proteins in canine organs (2,31,(39)(40)(41). Thus, in the present study, the organ-specific expression and localization of calcium (NCKX3, TRPV2), copper (CTR1, ATP7A), iron (IREG1) and ferroxidase for iron transporting (HEPH) proteins and mRNAs were investigated in the canine duodenum (upper part of the duodenum), kidney (borderline of the cortex and medulla), spleen (borderline of the white and red pulp) and liver (quadrate lobe of the liver).…”

Section: Discussionmentioning

confidence: 99%

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Organ‑specific expression of the divalent ion channel proteins NCKX3, TRPV2, CTR1, ATP7A, IREG1 and HEPH in various canine organs

2018

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Transmembrane cation channels include those for calcium, copper and iron ion transport. Each channel has physiological significance, and all have been associated with disease. However, the comparative study of transcriptional‑translational levels in canine organs has not been previously reported. In the present study, organ‑specific expression of calcium channels, including sodium/potassium/calcium exchanger 3 (NCKX3) and transient receptor potential cation channel subfamily V member 2 (TRPV2), copper channels, including high affinity copper uptake protein 1 (CTR1) and copper‑transporting ATPase 1 (ATP7A), and iron channels, including iron‑regulated transporter 1 (IREG1) and hephaestin (HEPH) proteins and their mRNAs were examined in the canine duodenum, kidney, spleen and liver. NCKX3 protein expression was highest in the kidney, moderate in the duodenum, and lowest in the spleen and liver, whereas TRPV2 protein was highly expressed in the kidney, duodenum and liver, and was low in the spleen. The CTR1 protein expression level was highest in the liver, followed (in descending order) by the duodenum, kidney and spleen. The ATP7A protein expression level was highest in the duodenum and lowest in the spleen. The IREG1 protein expression level was highest in the liver, followed (in descending order) by the kidney, duodenum and spleen. The HEPH protein level was high in liver, moderate in the duodenum and kidney, and low in the spleen. The results of the immunohistochemistry analysis demonstrated ion channel protein localizations. These results suggested that cation channel proteins are differentially expressed among canine organs, and they may be involved in organ‑specific functions associated with the maintenance of physiological homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Organ‑specific expression of the divalent ion channel proteins NCKX3, TRPV2, CTR1, ATP7A, IREG1 and HEPH in various canine organs

2018

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“…Urinalysis strips indicated that L-NAME mice exhibited obvious proteinuria (+ + ∼ + ++), and the control group showed absent to mild proteinuria. Previous studies have reported that elevated abundance of HIF1α is related to preeclamptic symptoms, and its level is increased not only in the placentas but also in circulation (3,27). Figure 2 demonstrates HIF1α abundance was indeed increased in the aortic tissues of PE mice (p < 0.01).…”

Section: Downregulation Of Crl3 Function and The Accumulation Of Wnk Kinases Pde5 And Rhoa In Placentas And Spiral Arteries Of Pe Patientmentioning

confidence: 74%

Downregulation of Cullin 3 Ligase Signaling Pathways Contributes to Hypertension in Preeclampsia

Zhang

Jiang

Zhang

2021

Front. Cardiovasc. Med.

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Background: Preeclampsia (PE) is a leading cause of maternal and perinatal morbidity and mortality; however, its etiology and pathophysiology remain obscure. PE is initiated by inadequate spiral artery remodeling and subsequent placental ischemia/hypoxia, which stimulates release of bioactive factors into maternal circulation, leading to hypertension and renal damage.Methods and Results: Abundance of key components of cullin 3-ring ubiquitin ligase (CRL3), including cullin 3 (CUL3) and its neddylated modification, and adaptors including Kelch-like 2 (KLHL2) and Rho-related BTB domain containing protein 1 was all decreased in spiral arteries and placentas of PE patients. Similar changes were found in aortic tissues and renal distal tubules of pregnant mice treated with Nω-nitro-l-arginine methyl ester hydrochloride. The downregulation of CRL3 function led to accumulation of with-no-lysine kinases, phosphodiesterase 5, and RhoA in vessels and renal distal tubules, which promoted vasoconstriction and Na–Cl cotransporter activation in the distal convoluted tubule (DCT), as well as vascular and DCT structure remodeling. Proton pump inhibitor esomeprazole partially restored CRL3 function. In vitro studies have shown that increased abundance of JAB1, a component of the COP9 signalosome, inhibited CUL3 neddylation and promoted the expression of hypoxia-inducible factor 1α, which downregulated peroxisome proliferator–activated receptor γ and further promoted CUL3 inactivation. KLHL3/2 was degraded by increased autophagy.Conclusion: These findings support that the downregulation of CRL3 function disrupts the balance of vasoconstriction and vasodilation and aggravates excess reabsorption of sodium in PE.

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“…This finding suggested a specific inhibitory effect of hypoxia on ecac expression. In rats, expression of the transient receptor potential vanilloid (TRPV) 5 and TRPV6 (orthologues of ECaC) was also found to decrease in the duodenum of animals exposed to hypoxia (Yang et al, 2013). In the present study, we also evaluated the effects of hypoxia on two hypocalcaemic hormones, stanniocalcin-1 (stc-1) and calcitonin (ct).…”

Section: Impact Of Hypoxia Exposure On Ionic Regulationmentioning

confidence: 92%

Inhibition of calcium uptake during hypoxia in developing zebrafish, Danio rerio, is mediated by hypoxia-inducible factor

Kwong

Kumai

Tzaneva

et al. 2016

Journal of Experimental Biology

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The present study investigated the potential role of hypoxia-inducible factor (HIF) in calcium homeostasis in developing zebrafish (Danio rerio). It was demonstrated that zebrafish raised in hypoxic water (30 mmHg; control, 155 mmHg P O2 ) until 4 days post-fertilization exhibited a substantial reduction in whole-body Ca 2+ levels and Ca 2+ uptake. Ca 2+ uptake in hypoxia-treated fish did not return to prehypoxia (control) levels within 2 h of transfer back to normoxic water. Results from real-time PCR showed that hypoxia decreased the whole-body mRNA expression levels of the epithelial Ca 2+ channel (ecac), but not plasma membrane Ca 2+ -ATPase ( pmca2) or Na + / Ca 2+ -exchanger (ncx1b). Whole-mount in situ hybridization revealed that the number of ecac-expressing ionocytes was reduced in fish raised in hypoxic water. These findings suggested that hypoxic treatment suppressed the expression of ecac, thereby reducing Ca 2+ influx. To further evaluate the potential mechanisms for the effects of hypoxia on Ca 2+ regulation, a functional gene knockdown approach was employed to prevent the expression of HIF-1αb during hypoxic treatment. Consistent with a role for HIF-1αb in regulating Ca 2+ balance during hypoxia, the results demonstrated that the reduction of Ca 2+ uptake associated with hypoxic exposure was not observed in fish experiencing HIF-1αb knockdown. Additionally, the effects of hypoxia on reducing the number of ecac-expressing ionocytes was less pronounced in HIF-1αb-deficient fish. Overall, the current study revealed that hypoxic exposure inhibited Ca 2+ uptake in developing zebrafish, probably owing to HIF-1αb-mediated suppression of ecac expression.

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Change of Genes in Calcium Transport Channels Caused by Hypoxic Stress in the Placenta, Duodenum, and Kidney of Pregnant Rats1

Cited by 16 publications

References 81 publications

Organ‑specific expression of the divalent ion channel proteins NCKX3, TRPV2, CTR1, ATP7A, IREG1 and HEPH in various canine organs

Organ‑specific expression of the divalent ion channel proteins NCKX3, TRPV2, CTR1, ATP7A, IREG1 and HEPH in various canine organs

Downregulation of Cullin 3 Ligase Signaling Pathways Contributes to Hypertension in Preeclampsia

Inhibition of calcium uptake during hypoxia in developing zebrafish, Danio rerio, is mediated by hypoxia-inducible factor

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