title: Upregulation of Bpifb1 expression in the parotid glands of non-obese diabetic mice.
abstract: OBJECTIVE
  To define the increased mRNA expression of Bpifb1, a member of the bactericidal/permeability-increasing protein family, in parotid acinar cells from non-obese diabetic (NOD) mice, an animal model for Sjögren's syndrome.
  
  
  METHODS
  Parotid acinar cells were prepared from female NOD (NOD/ShiJcl) mice with or without diabetes, as well as from control (C57BL/6JJcl) mice. Total RNA and homogenate were prepared from the parotid acinar cells. Embryonic cDNA from a Mouse MTC(™) Panel I kit was used. The expression of Bpifb1 was determined by cDNA microarray analysis, RT-PCR, real-time PCR, northern blotting and in situ hybridization.
  
  
  RESULTS
  The expression of Bpifb1 mRNA was high in parotid acinar cells from diabetic and non-diabetic NOD mice at 5-50 weeks of age. Acinar cells in the C57BL/6 mice had a low expression of Bpifb1 mRNA at an age >8 weeks, but had a relatively high expression in the foetus and infantile stages.
  
  
  CONCLUSIONS
  Bpifb1 mRNA is upregulated in parotid acinar cells in NOD mice, but its expression is not related to the onset of diabetes. These findings suggest that high expression levels of Bpifb1 might predict disease traits before the onset of autoimmunity.
authors.affiliation: Departments of Biochemistry, The Nippon Dental University School of Life Dentistry at Niigata, Chuo-ku, Niigata, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nashida
authors.affiliation: Departments of Anatomy, The Nippon Dental University School of Life Dentistry at Niigata, Chuo-ku, Niigata, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yoshimura
authors.affiliation: Departments of Histology, The Nippon Dental University School of Life Dentistry at Niigata, Chuo-ku, Niigata, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Yoshie
authors.affiliation: Departments of Removable Prosthodontics, The Nippon Dental University School of Life Dentistry at Niigata, Chuo-ku, Niigata, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Mizuhashi
authors.affiliation: Departments of Pediatric Dentistry, The Nippon Dental University School of Life Dentistry at Niigata, Chuo-ku, Niigata, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Shimomura-Kuroki
mesh_terms: D061354:Acinar Cells / Q000378:metabolism; D000818:Animals; D015152:Blotting, Northern / Q000379:methods; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000235:genetics; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D017403:In Situ Hybridization / Q000379:methods; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016688:Mice, Inbred NOD; D010306:Parotid Gland / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D012859:Sjogren's Syndrome / Q000378:metabolism; D015854:Up-Regulation
chemical_list: C579352:BPIFB1 protein, mouse; D002352:Carrier Proteins; D012333:RNA, Messenger
keywords: Bpifb1; NOD mouse; parotid acinar cells