PUBLICATION

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

Authors
Kwong, R.W., Kumai, Y., Tzaneva, V., Azzi, E., Hochhold, N., Robertson, C., Pelster, B., Perry, S.F.
ID
ZDB-PUB-161102-3
Date
2016
Source
The Journal of experimental biology   219(Pt 24): 3988-3995 (Journal)
Registered Authors
Pelster, Bernd, Perry, Steve F.
Keywords
Calcium, ECaC, Ion regulation, HIF, fish, Ionocyte
MeSH Terms
  • Hypoxia/metabolism*
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Biological Transport/drug effects
  • Biological Transport/genetics
  • Cell Count
  • Protein Stability/drug effects
  • Animals
  • Ions
  • Gene Knockdown Techniques
  • TRPV Cation Channels/genetics
  • TRPV Cation Channels/metabolism
  • Calcium/metabolism*
  • Morpholinos/pharmacology
  • Hypoxia-Inducible Factor 1, alpha Subunit/metabolism*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Gene Expression Regulation/drug effects
(all 20)
PubMed
27802147 Full text @ J. Exp. Biol.
Abstract
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 PO2 ) until 4 days post-fertilization exhibited a substantial reduction in whole-body Ca2+ levels and Ca2+ uptake. Ca2+ uptake in hypoxia-treated fish did not return to pre-hypoxia (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 Ca2+ channel (ecac), but not plasma membrane Ca2+-ATPase (pmca2) or Na+/Ca2+-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 Ca2+ influx. To further evaluate the potential mechanisms for the effects of hypoxia on Ca2+ 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 Ca2+ balance during hypoxia, the results demonstrated that the reduction of Ca2+ 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 Ca2+ uptake in developing zebrafish, probably owing to HIF-1αb-mediated suppression of ecac expression.
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Citation
Kwong, R.W., Kumai, Y., Tzaneva, V., Azzi, E., Hochhold, N., Robertson, C., Pelster, B., Perry, S.F. (2016) Inhibition of calcium uptake during hypoxia in developing zebrafish, is mediated by hypoxia-inducible factor. The Journal of experimental biology. 219(Pt 24):3988-3995.