Editorial
Copyright ©2010 Baishideng.
World J Gastroenterol. May 14, 2010; 16(18): 2195-2201
Published online May 14, 2010. doi: 10.3748/wjg.v16.i18.2195
Table 1 Identified roles of SRF in the GI tract
GI systemProcess involvedMolecules associatedGI disorder associated
EsophagusMyofibroblast differentiation[19]TGFβ, ILKUlcer
StomachAngiogenesis[20]VEGF, Rho-actin, MEK-ERKUlcer
StomachRe-epithelialization, muscular structure restoration[6]Actin, immediate-early genesUlcer
StomachH. pylori activates SRF[21,22]CagA, villinIntestinal metaplasia
IntestineSmooth muscle contraction[23,24]Smooth muscle actin, smooth muscle myosin, smoothelin, F/G actinIntestinal obstruction, CIPO
ColonAlternative splicing, cell survival[26]SRFΔ5, K-rasColon cancer
LiverCell cycle; hepatocyte proliferation/survival[29,30]IGF-1Liver injury
LiverCell proliferation, cell cycle, apoptosis[33]E2F1Hepatocellular carcinoma
LiverCell invasion[31]E-cadherin, β-cateninLiver metastasis
PancreasCell proliferation[32]Pro-inflammatory cytokinesPancreatitis
Table 2 Tools and models available to study SRF functions in GI
ToolPurposeModel
SRF in pcDNA3.1, His[6,21]SRF over-expressionGene therapy
SRF antisense sequence[21,33]SRF down-regulation (siRNA)Gene depletion
Srf Flex1 mice[35]Conditional in vivo SRF deletionGene depletion
Srf loxP mice[30]Conditional in vivo SRF deletionGene depletion
CreER T2 mice[36]SMS tissue expressionCIPO
AlfpCre mice[31]Hepatocyte tissue expressionLiver function
K5-Cre mice[37]Squamous epithelial expressionEsophagus, foregut
Fabp/Cre mice[38]Conditional gut tissue expressionSmall/large intestine
H. pylori[23]H. pylori infection in human cell lines (in vitro) or mice (in vivo)H. pylori gastric diseases