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Distribution and dynamics of branchial ionocytes in houndshark reared in full-strength and diluted seawater environments.

Abstract

In teleost fishes, it is well-established that the gill serves as an important ionoregulatory organ in addition to its primary function of respiratory gas exchange. In elasmobranchs, however, the ionoregulatory function of the gills is still incompletely understood. Although two types of ionocytes, Na(+)/K(+)-ATPase (NKA)-rich (type-A) cell and vacuolar-type H(+)-ATPase (V-ATPase)-rich (type-B) cell, have been found in elasmobranch fishes, these cells were considered to function primarily in acid-base regulation. In the present study, we examined ion-transporting proteins expressed in ionocytes of Japanese-banded houndshark, Triakis scyllium, reared in full-strength seawater (SW) and transferred to diluted (30%) SW. In addition to the upregulation of NKA and Na(+)/H(+) exchanger type 3 (NHE3) mRNAs in the type-A ionocytes, we found that Na(+), Cl(-) cotransporter (NCC, Slc12a3) is expressed in a subpopulation of the type-B ionocytes, and that the expression level of NCC mRNA was enhanced in houndsharks transferred to a low-salinity environment. These results suggest that elasmobranch gill ionocytes contribute to NaCl uptake in addition to the already described function of acid-base regulation, and that NCC is most probably one of the key molecules for hyper-osmoregulatory function of elasmobranch gills. The existence of two types of ionocytes (NHE3- and NCC-expressing cells) that are responsible for NaCl absorption seems to be a common feature in both teleosts and elasmobranchs for adaptation to a low salinity environment. A possible driving mechanism for NCC in type-B ionocytes is discussed.

Authors+Show Affiliations

Laboratory of Physiology, Atmosphere and Ocean Research Institute, University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba 277-8564, Japan. Electronic address: takabe@aori.u-tokyo.ac.jp.Laboratory of Physiology, Atmosphere and Ocean Research Institute, University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba 277-8564, Japan.Laboratory of Physiology, Atmosphere and Ocean Research Institute, University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba 277-8564, Japan; Hawai'i Institute of Marine Biology, University of Hawai'i, 46-007 Lilipuna Road, Kaneohe, HI 96744, USA.Laboratory of Physiology, Atmosphere and Ocean Research Institute, University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba 277-8564, Japan.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27040185

Citation

Takabe, Souichirou, et al. "Distribution and Dynamics of Branchial Ionocytes in Houndshark Reared in Full-strength and Diluted Seawater Environments." Comparative Biochemistry and Physiology. Part A, Molecular & Integrative Physiology, vol. 198, 2016, pp. 22-32.
Takabe S, Inokuchi M, Yamaguchi Y, et al. Distribution and dynamics of branchial ionocytes in houndshark reared in full-strength and diluted seawater environments. Comp Biochem Physiol A Mol Integr Physiol. 2016;198:22-32.
Takabe, S., Inokuchi, M., Yamaguchi, Y., & Hyodo, S. (2016). Distribution and dynamics of branchial ionocytes in houndshark reared in full-strength and diluted seawater environments. Comparative Biochemistry and Physiology. Part A, Molecular & Integrative Physiology, 198, 22-32. https://doi.org/10.1016/j.cbpa.2016.03.019
Takabe S, et al. Distribution and Dynamics of Branchial Ionocytes in Houndshark Reared in Full-strength and Diluted Seawater Environments. Comp Biochem Physiol A Mol Integr Physiol. 2016;198:22-32. PubMed PMID: 27040185.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Distribution and dynamics of branchial ionocytes in houndshark reared in full-strength and diluted seawater environments. AU - Takabe,Souichirou, AU - Inokuchi,Mayu, AU - Yamaguchi,Yoko, AU - Hyodo,Susumu, Y1 - 2016/03/31/ PY - 2016/01/04/received PY - 2016/03/18/revised PY - 2016/03/23/accepted PY - 2016/4/5/entrez PY - 2016/4/5/pubmed PY - 2017/6/14/medline KW - Elasmobranch KW - Gill KW - Houndshark KW - Ionocytes KW - Ionoregulation KW - Na(+), Cl(−) cotransporter SP - 22 EP - 32 JF - Comparative biochemistry and physiology. Part A, Molecular & integrative physiology JO - Comp Biochem Physiol A Mol Integr Physiol VL - 198 N2 - In teleost fishes, it is well-established that the gill serves as an important ionoregulatory organ in addition to its primary function of respiratory gas exchange. In elasmobranchs, however, the ionoregulatory function of the gills is still incompletely understood. Although two types of ionocytes, Na(+)/K(+)-ATPase (NKA)-rich (type-A) cell and vacuolar-type H(+)-ATPase (V-ATPase)-rich (type-B) cell, have been found in elasmobranch fishes, these cells were considered to function primarily in acid-base regulation. In the present study, we examined ion-transporting proteins expressed in ionocytes of Japanese-banded houndshark, Triakis scyllium, reared in full-strength seawater (SW) and transferred to diluted (30%) SW. In addition to the upregulation of NKA and Na(+)/H(+) exchanger type 3 (NHE3) mRNAs in the type-A ionocytes, we found that Na(+), Cl(-) cotransporter (NCC, Slc12a3) is expressed in a subpopulation of the type-B ionocytes, and that the expression level of NCC mRNA was enhanced in houndsharks transferred to a low-salinity environment. These results suggest that elasmobranch gill ionocytes contribute to NaCl uptake in addition to the already described function of acid-base regulation, and that NCC is most probably one of the key molecules for hyper-osmoregulatory function of elasmobranch gills. The existence of two types of ionocytes (NHE3- and NCC-expressing cells) that are responsible for NaCl absorption seems to be a common feature in both teleosts and elasmobranchs for adaptation to a low salinity environment. A possible driving mechanism for NCC in type-B ionocytes is discussed. SN - 1531-4332 UR - https://www.unboundmedicine.com/medline/citation/27040185/Distribution_and_dynamics_of_branchial_ionocytes_in_houndshark_reared_in_full_strength_and_diluted_seawater_environments_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1095-6433(16)30064-2 DB - PRIME DP - Unbound Medicine ER -