Tissue-specific expression of calcium channels

Hullin, Roger; Biel, Martin; Flockerzi, Veit; Hofmann, Franz

doi:10.1016/1050-1738(93)90036-6

Cited by 36 publications

(9 citation statements)

References 52 publications

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“…5A and 5B showed that the expressions of both α1c and β2c subunits in hypertrophic ventricle were significantly less than those in control group, however, the expression of α2/δ subunit was constant. α1c subunit is the pore-forming subunit and dictates the basic electrophysiological characteristics of the channel, such as ion selectivity, conductivity and the activation threshold of the channel [33,34] and our electrophysiological finding was consistent with their result that α1c subunits expression was reduced in post-MI hypertrophyic cardiomyocytes, suggesting that I CaL density in post-MI hypertrophyic cardiomyocyte are decreased dramatically. The β subunit regulates the amplitude of the calcium inward current and influence the calcium inward current inactivation.…”

Section: Discussionsupporting

confidence: 91%

“…The β subunit regulates the amplitude of the calcium inward current and influence the calcium inward current inactivation. There are 3 kinds of β subunits expressed in human ventricle, including β1, β2 and β3 [33,[35][36][37][38][39] . It has been proved that the expression of β1 subunit was decreased by about 70% at mRNA level in cardiomyocyte of diastolic failing heart although there were not alterations of α1c and α2/δ mRNA expression found at that stage [40] .…”

Section: Discussionmentioning

confidence: 99%

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Abnormal calcium “Sparks” in cardiomyocytes of post-myocardial infarction heart

Huang

et al. 2008

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6 weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of I(CaL) decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alpha1c, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant. It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes, which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Abnormal calcium “Sparks” in cardiomyocytes of post-myocardial infarction heart

Huang

et al. 2008

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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“…For example, the a10 primers were patterned after regions within the conserved nucleotide sequences corresponding to the putative transmembrane regions S4 and S6 within the third repeat of the channel protein ( Fig. 1A; Tanabe et al, 1987), thus encompassing a presumptive voltage sensor (Hullin et al, 1993). In a similar manner, separate primers were designed to amplify each of the other a1 subunits (alA,~atc, and ais).…”

Section: Methodsmentioning

confidence: 99%

“…VGCCs include the L-type, N-type, P-type, and Ttype, with classifications based on pharmacologic sensitivities to channel blockers and activators as well as electrophysiologic characteristics (Nowycky et al, 1985;Fox et al, l987a,b;Mintz et al, 1992;Zhang et al, 1993). L-type calcium channels are voltagegated ion channels that are sensitive to dihydropyridines and phenylalkylamines (reviewed by Tsien et al, 1987;Bean, 1989;Hess, 1990;Hullin et al, 1993). N-type channels are specifically inhibited by w-conotoxin GVIA (Herdon and Nahorski, 1989).…”

Section: Introductionmentioning

confidence: 99%

Calcium Channel Subunits in the Mouse Cochlea

Green¹,

Khan

Beisel

et al. 1996

Journal of Neurochemistry

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Messages for subunits of voltage-gated calcium channels were examined in the cochlea of the CBAm ouse by PCR analysis. Total RNA was extracted from the auditory organs of 16-18-day-old animals. After reverse transcription, resulting cDNA was amplified by PCR with primers targeted to nucleotide sequences corresponding to 12 different calcium channel subunits. PCR products representing subunit gene expression were strongly and consistently amplified for aic, a 10, alE, /3~,/33, and /3~but not for alA, aiB, ais, /32, or y. The chosen primers amplified cochlear cDNA to yield an overall pattern of bands different from that of any tissue studied thus far, in particular with respect to the a25 and /3s ubunits; the a26 product was found to be significantly shorter than the corresponding brain and skeletal muscle isoforms. Nucleotide sequencing confirmed the identity of mouse cochlear subunit cDNAs. The results suggest that L-type and presumptive R-type calcium channels are expressed in the mammalian cochlea and that the a25 subunits may be coded by a characteristic splice-variant mRNA.

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“…The VGCCs are assembled from 3 tissue-specific isoforms of a 1 (a 1 1.2), a 2 d 1 , and b (largely the b 2 and b 3 isoforms) while the g subunit is only present in skeletal muscle Hullin et al, 1992). The a 1 subunit contains the binding site for Ca 21 -channel antagonists such as dihydropiridines, phenylalkylamines, and benzodiacepines and is responsible for voltage-gated Ca 21 movement through the sarcolemma Hullin et al, 1993;Tuana and Murphy, 1990). Depolarization of cardiac myocytes is suggested to lead to the opening of the L-type calcium channels with Ca 21 influx through the VGCCs, stimulating the opening of the RyR 2 and resulting in a cascade of Ca 21 ions released into the cytosol, i.e.…”

mentioning

confidence: 99%