Rodent IRR-219 (IgGFcgammaBP) and rTFF3, expressed mainly in the intestinal mucosa, depleted during dextran sulfate sodium-induced colitis.
IgGFcgammaBP and TFF3 are related with adaptation during injury, mucosal defense, and epithelial healing. In this work, we produced the polyclonal antibodies for rat IgGFcgammaBP or TFF3 and assessed their tissue distributions in adult and prenatal rats, rTFF3 molecular patterns under reduced and nonreduced condition, involvement of IgGFcgammaBP, and TFF3 in dextran sulfate sodium (DSS)-induced colitis. Polyclonal antibodies of rat IgGFcgammaBP or TFF3 were produced with their synthetic polypeptide. Rat TFF3 was detected in the scraped intestinal mucosa by SDS/PAGE and Western blotting. Immunohistochemical stainings of rat IgGFcgammaBP or TFF3 were performed in different tissues, mainly in mucin-producing tissues, of adult rat and prenatal rat intestine. Rat IgGFcgammaBP and TFF3 were immunohistochemically detected in the distal colon of rat colitis model induced with 7% DSS. IgGFcgammaBP and TFF3 were mainly expressed in the intestinal mucosa with different distribution patterns. The scattered staining was also found in the epithelium of bile duct. There was strong expression of IgGFcgammaBP and TFF3 in rat embryonic intestine. There were two kinds of rTFF3 complexes existed with different molecular weights, 250 and 55 kDa, under nonreduced conditions, but shifted to 6 kDa under reduced conditions. In the DSS-induced colitis model, IgGFcgammaBP and TFF3 were significantly decreased in the distal colon mucosa at the onset and active phases comparing with the normal control, partially recovered at the regenerative phase. Based on these findings,IgGFcgammaBP and TFF3 were widely expressed in the intestinal mucosa, depleted during DSS-induced colitis. Rat TFF3 existed mainly in two complexes with 250 and 55 kDa molecular weights. The present findings indicate they are two important goblet cell-derived components possibly related to the pathogenesis of DSS-induced colitis, a rat model of ulcerative colitis.
Feng
Zao-Ming
ZM
Department of Gastroenterology, Southwestern Hospital, Third Military Medical University, Chongqing 400038, People's Republic of China.
Fang
Dian-Chun
DC
Chen
Wen-Sheng
WS
Wang
Rong-Quan
RQ
D000818:Animals; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics*; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D003106:Colon / Q000187:drug effects / Q000196:embryology / Q000378:metabolism; D016264:Dextran Sulfate / Q000633:toxicity; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015870:Gene Expression; D018507:Gene Expression Regulation, Developmental; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009479:Neuropeptides / Q000096:biosynthesis / Q000235:genetics*; D010952:Plasma Substitutes / Q000633:toxicity; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D000071165:Trefoil Factor-3
D002352:Carrier Proteins; C416187:IRR-219 protein, rat; D009479:Neuropeptides; D010952:Plasma Substitutes; D012333:RNA, Messenger; C099037:TFF3 protein, rat; D000071165:Trefoil Factor-3; D016264:Dextran Sulfate