Estradiol regulation in porto-sinusoidal vascular disease (Homo sapiens)

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Bibliography

1. Gu M, Zhu Y, Yin X, Zhang DM; ''Small-conductance Ca²⁺-activated K⁺channels: insights into their roles in cardiovascular disease.''; Exp Mol Med, 2018 PubMed Europe PMC Scholia
2. Griffon N, Schuers M, Dhombres F, Merabti T, Kerdelhué G, Rollin L, Darmoni SJ; ''Searching for rare diseases in PubMed: a blind comparison of Orphanet expert query and query based on terminological knowledge.''; BMC Med Inform Decis Mak, 2016 PubMed Europe PMC Scholia
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4. Morikawa H, Morrisett RA; ''Ethanol action on dopaminergic neurons in the ventral tegmental area: interaction with intrinsic ion channels and neurotransmitter inputs.''; Int Rev Neurobiol, 2010 PubMed Europe PMC Scholia
5. Schouten JN, Garcia-Pagan JC, Valla DC, Janssen HL; ''Idiopathic noncirrhotic portal hypertension.''; Hepatology, 2011 PubMed Europe PMC Scholia
6. Taylor MS, Bonev AD, Gross TP, Eckman DM, Brayden JE, Bond CT, Adelman JP, Nelson MT; ''Altered expression of small-conductance Ca2+-activated K+ (SK3) channels modulates arterial tone and blood pressure.''; Circ Res, 2003 PubMed Europe PMC Scholia
7. Weisbrod D; ''Small and Intermediate Calcium Activated Potassium Channels in the Heart: Role and Strategies in the Treatment of Cardiovascular Diseases.''; Front Physiol, 2020 PubMed Europe PMC Scholia
8. Ledoux J, Werner ME, Brayden JE, Nelson MT; ''Calcium-activated potassium channels and the regulation of vascular tone.''; Physiology (Bethesda), 2006 PubMed Europe PMC Scholia
9. Besmond C, Valla D, Hubert L, Poirier K, Grosse B, Guettier C, Bernard O, Gonzales E, Jacquemin E; ''Mutations in the novel gene FOPV are associated with familial autosomal dominant and non-familial obliterative portal venopathy.''; Liver Int, 2018 PubMed Europe PMC Scholia
10. Sith Siramolpiwat, Susana Seijo; ''Idiopathic non-cirrhotic portal hypertension''; Journal of Rare Diseases Research & Treatment, 2016
11. Köhler M, Hirschberg B, Bond CT, Kinzie JM, Marrion NV, Maylie J, Adelman JP; ''Small-conductance, calcium-activated potassium channels from mammalian brain.''; Science, 1996 PubMed Europe PMC Scholia
12. Jacobson D, Pribnow D, Herson PS, Maylie J, Adelman JP; ''Determinants contributing to estrogen-regulated expression of SK3.''; Biochem Biophys Res Commun, 2003 PubMed Europe PMC Scholia
13. Köhler R, Ruth P; ''Endothelial dysfunction and blood pressure alterations in K+-channel transgenic mice.''; Pflugers Arch, 2010 PubMed Europe PMC Scholia
14. Koot BG, Alders M, Verheij J, Beuers U, Cobben JM; ''A de novo mutation in KCNN3 associated with autosomal dominant idiopathic non-cirrhotic portal hypertension.''; J Hepatol, 2016 PubMed Europe PMC Scholia
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16. Pierce SL, England SK; ''SK3 channel expression during pregnancy is regulated through estrogen and Sp factor-mediated transcriptional control of the KCNN3 gene.''; Am J Physiol Endocrinol Metab, 2010 PubMed Europe PMC Scholia

History

External references

DataNodes

Name	Type	Database reference	Comment
Apamin	Metabolite	16133797 (PubChem-compound)	The SK3 channel is apamin sensitive. The peptide toxin apamin, present in bee venom, blocks the SK3 channels, reducing hyperpolarization of the cells (Morikawa, 2010; Weisbrod, 2020)
CALM1	Protein	P0DP23 (Uniprot-TrEMBL)
Ca2+	Metabolite	CHEBI:29108 (ChEBI)
ESR1	Protein	P03372 (Uniprot-TrEMBL)
Endothelial derived hyperpolarization (EDH) of vascular smooth muscle cells		Q1355864 (Wikidata)
Endothelial hyperpolarization		Q1355864 (Wikidata)
Estradiol	Metabolite	CHEBI:16469 (ChEBI)
K+	Metabolite	CHEBI:29103 (ChEBI)
KCNN3	GeneProduct	ENSG00000143603 (Ensembl)	A single nucleotide substitution (SNP) c.1348G>C in the KCNN3 gene was found in a father with INCPH and three of his children that were tested with Sanger- and whole-exome sequencing. These three children had developed signs of INCPH in the first ten years of their lives. A full sister of one of the girls had no complaints and did not participate in the examinations. Ultrasound and liver tests of the paternal grandparents showed no abnormalities of the liver. (Koot et al. 2015) KCNN genes are expressed in neurons, epithelium, endothelium of the vasculature, and several types of smooth muscle. The SK3 channel, which is a gene product of the KCNN3 gene, is involved in vascular tone- and blood pressure regulation. Calcium-induced activation of the SK3 channel will cause hyperpolarization of endothelial cells, resulting in hyperpolarization of the adjacent muscle cell, which is also known as an endothelium-derived hyperpolarizing factor (EDHF). This hyperpolarization of the muscle cells will then result in dilation in resistance arteries (Ledoux et al. 2006; Kohler et al. 2010). The level of SK3 channel expression in endothelial cells was found to be important for vascular tone and blood pressure in mice. (Taylor et al. 2003) Gene transcription: Two binding sites for the SP1 and SP3 transcription factors are present in the promotor region of the KCNN3 gene in mice. SP1 and SP3 compete to regulate the expression of the KCNN3 gene, influenced by the environment of the promotors. SP1 activates the expression of the gene, and SP3 inhibits the expression of the gene (Pierce et al., 2010; Xiong et al., 2020) . It was found that ERα stimulates the transcription KCNN3 through these transcription factors (Jacobson et al., 2003).
Lower blood pressure		Q275419 (Wikidata)
SK3	Protein	Q9UGI6 (Uniprot-TrEMBL)	Also referred to as: Small-conductance Ca2+- activated K+ (SK) channel Small conductance calcium-activated potassium channel protein 3 SK3 channel SKCa 3 KCa channel About: The SK3 channel is important for afterhyperpolarization following an action potential. One channel is made from four monomers which all contain six transmembrane segments, connected via a single pore loop. The N-termini and the C-termini are both located at the intracellular side of the membrane. A calmodulin molecule is located at the C-termini of the SK3 channel via a CaM-binding domain. Calmodulin will activate the SK3 channel upon binding of Ca2+. SK3 channels are not voltage-dependent. (Gu et al. 2018; Köhler et al. 1996; Weisbrod, 2020) Calcium-induced activation of the SK3 channel will cause hyperpolarization of endothelial cells, resulting in hyperpolarization of the adjacent muscle cell, which is also known as an endothelium-derived hyperpolarizing factor (EDHF). This hyperpolarization of the muscle cells will then result in dilation in resistance arteries (Ledoux et al. 2006; Kohler et al. 2010). The level of SK3 channel expression in endothelial cells was found to be important for vascular tone and blood pressure in mice. (Taylor et al. 2003)
SP1	Protein	P08047 (Uniprot-TrEMBL)
SP3	Protein	Q02447 (Uniprot-TrEMBL)
Vascular dilation		Q14859627 (Wikidata)

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