Increase in pro-apoptotic Bax expression and decrease in anti-apoptotic Bcl-2 expression in newborns with necrotizing enterocolitis.

BACKGROUND/AIM The aim of the present study was to find out if there is an increase in the expression of pro-apoptotic Bax and reduction in expression of anti-apoptotic Blc-2A1 in newborn intestines with necrotizing enterocolitis (NEC). MATERIALS AND METHODS We compared 8 consecutive newborn patients undergoing bowel resection for NEC with 8 neonates undergoing intestinal resection for ileal atresia. Histopathological evaluation of tissue injury and apoptosis was performed by using light microscopic examination and TUNEL method. The mRNA level of apoptotic (CASP3, CASP6, CASP7, Bax, BIRC2) and anti-apoptotic genes were evaluated by PCR array method. Protein expression was assessed by immunohistochemistry. RESULTS We compared 8 consecutive newborn patients undergoing bowel resection for NEC with 8 neonates undergoing intestinal resection for ileal atresia. Histopathological evaluation of tissue injury and apoptosis was performed by using light microscopic examination and TUNEL method. The mRNA level of apoptotic (CASP3, CASP6, CASP7, Bax, BIRC2) and anti-apoptotic genes were evaluated by PCR array method. Protein expression was assessed by immunohistochemistry. CONCLUSIONS Our data in humannewborns suggest that alteration of the balance between pro-apoptotic Bax expression and anti-apoptotic Bcl-2A1 expression in the site of injury is a possible mechanism in the pathogenesis of NEC.

[1]  W. Zhou,et al.  Glutamine downregulates TLR-2 and TLR-4 expression and protects intestinal tract in preterm neonatal rats with necrotizing enterocolitis. , 2014, Journal of pediatric surgery.

[2]  S. Walters,et al.  Quality of life in children and adolescents with Osteogenesis Imperfecta: a qualitative interview based study , 2014, Health and Quality of Life Outcomes.

[3]  D. Sillence,et al.  Osteogenesis imperfecta: Clinical diagnosis, nomenclature and severity assessment , 2014, American journal of medical genetics. Part A.

[4]  Peter E. Czabotar,et al.  Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy , 2013, Nature Reviews Molecular Cell Biology.

[5]  M. D. Pino,et al.  Osteogénesis imperfecta: estudio de la calidad de vida en los niños , 2013 .

[6]  J. Marini,et al.  New genes in bone development: what's new in osteogenesis imperfecta. , 2013, The Journal of clinical endocrinology and metabolism.

[7]  T. Delibaşı,et al.  TSH-induced gene expression involves regulation of self-renewal and differentiation-related genes in human bone marrow-derived mesenchymal stem cells. , 2012, The Journal of endocrinology.

[8]  F. Glorieux,et al.  Genotype-Phenotype Correlations in Autosomal Dominant Osteogenesis Imperfecta , 2011, Journal of osteoporosis.

[9]  F. Glorieux,et al.  Activities and participation in young adults with osteogenesis imperfecta. , 2011, Journal of pediatric rehabilitation medicine.

[10]  M. Halpern,et al.  Bifidobacterium bifidum reduces apoptosis in the intestinal epithelium in necrotizing enterocolitis. , 2010, American journal of physiology. Gastrointestinal and liver physiology.

[11]  A. Maheshwari,et al.  Epidermal growth factor reduces autophagy in intestinal epithelium and in the rat model of necrotizing enterocolitis. , 2010, American journal of physiology. Gastrointestinal and liver physiology.

[12]  H. Correa,et al.  Apical sodium-dependent bile acid transporter upregulation is associated with necrotizing enterocolitis. , 2010, American journal of physiology. Gastrointestinal and liver physiology.

[13]  M. D. Pino,et al.  Osteogénesis imperfecta: Evaluación clínica, funcional y multidisciplinaria de 65 pacientes , 2010 .

[14]  T. Shakespeare,et al.  Medical and social aspects of the life course for adults with a skeletal dysplasia: A review of current knowledge , 2008, Disability and rehabilitation.

[15]  D. Hackam,et al.  A Critical Role for TLR4 in the Pathogenesis of Necrotizing Enterocolitis by Modulating Intestinal Injury and Repair1 , 2007, The Journal of Immunology.

[16]  Jessica A Clark,et al.  Reduction of experimental necrotizing enterocolitis with anti-TNF-alpha. , 2006, American journal of physiology. Gastrointestinal and liver physiology.

[17]  Y. Vodovotz,et al.  Intestinal and hepatic expression of BNIP3 in necrotizing enterocolitis: regulation by nitric oxide and peroxynitrite. , 2005, American journal of physiology. Gastrointestinal and liver physiology.

[18]  Catherine S. Williams,et al.  Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis. , 2005, American journal of physiology. Gastrointestinal and liver physiology.

[19]  M. Caplan,et al.  Intestinal Epithelial Apoptosis Initiates Gross Bowel Necrosis in an Experimental Rat Model of Neonatal Necrotizing Enterocolitis , 2004, Pediatric Research.

[20]  F. Bertucci,et al.  Immunophenotypic analysis of inflammatory breast cancers: identification of an ‘inflammatory signature’ , 2004, The Journal of pathology.

[21]  B. Dvořák,et al.  Epidermal growth factor and necrotizing enterocolitis. , 2004, Clinics in perinatology.

[22]  L. Root,et al.  Quality of life in osteogenesis imperfecta , 2001, International Orthopaedics.

[23]  H. Ford,et al.  The role of inflammatory cytokines and nitric oxide in the pathogenesis of necrotizing enterocolitis. , 1997, Journal of pediatric surgery.

[24]  B. Wright,et al.  Structure of a combination of Functional Independence Measure and Instrumental Activity Measure items in community-living persons: a study of individuals with cerebral palsy and spina bifida. , 1996, Archives of physical medicine and rehabilitation.

[25]  D. Cole Psychosocial aspects of osteogenesis imperfecta: an update. , 1993, American journal of medical genetics.

[26]  P. Noone,et al.  NECROTISING ENTEROCOLITIS , 1977, The Lancet.