Journal
JOURNAL OF PHYSIOLOGICAL SCIENCES
Volume 60, Issue 1, Pages 9-17Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s12576-009-0068-0
Keywords
Calcium absorption; Small interfering RNA (siRNA); Transcellular transport; Triple knockdown; Voltage-dependent calcium channel (Ca-v)
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Funding
- Mahidol University [SCY52-02, SCR52-01]
- Commission on Higher Education
- Thailand Research Fund [RSA5180001, RTA5080008]
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The milk-producing hormone prolactin (PRL) increases the transcellular intestinal calcium absorption by enhancing apical calcium uptake through voltage-dependent L-type calcium channel (Ca-v) 1.3. However, the redundancy of apical calcium channels raised the possibility that Ca(v)1.3 may operate with other channels, especially transient receptor potential vanilloid family calciumchannels (TRPV) 5 or 6, in an interdependent manner. Herein, TRPV5 knockdown (KD), TRPV5/TRPV6, TRPV5/Ca(v)1.3, and TRPV6/Ca(v)1.3 double KD, and TRPV5/TRPV6/Ca(v)1.3 triple KD Caco-2 monolayers were generated by transfecting cells with small interfering RNAs (siRNA). siRNAs downregulated only the target mRNAs, and did not induce compensatory upregulation of the remaining channels. After exposure to 600 ng/mL PRL, the transcellular calcium transport was increased by similar to 2-fold in scrambled siRNA-treated, TRPV5 KD and TRPV5/TRPV6 KD monolayers, but not in TRPV5/Ca(v)1.3, TRPV6/Ca(v)1.3 and TRPV5/TRPV6/Ca(v)1.3 KD monolayers. The results suggested that Ca(v)1.3 was the sole apical channel responsible for the PRL-stimulated transcellular calcium transport in intestine-like Caco-2 monolayer.
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