Title : Zinc deficiency promotes cystitis-related bladder pain by enhancing function and expression of Cav3.2 in mice.

Pub. Date : 2018 Jan 15

PMID : 29129814






9 Functional Relationships(s)
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1 The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice. Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
2 The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice. Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
3 Acute zinc deficiency caused by systemic N,N,N",N"-tetrakis-(2-pyridylmethyl)-ethylendiamine (TPEN), a zinc chelator, mimicked the dietary zinc deficiency-induced Cav3.2-dependent promotion of BP/RH following CPA at 200mg/kg. Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
4 CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG). Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
5 CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG). Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
6 CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG). Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
7 CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG). Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
8 The CSE inhibitor, beta-cyano-l-alanine, prevented the BP/RH and upregulation of Cav3.2, Egr-1 and USP5 in DRG following TPEN plus CPA at 200mg/kg. Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
9 Together, zinc deficiency promotes bladder pain accompanying CPA-induced cystitis by enhancing function and expression of Cav3.2 in nociceptors, suggesting a novel therapeutic avenue for treatment of bladder pain, such as zinc supplementation. Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus