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Immunohistochemical Studies of Age-Related Changes in Cell Proliferation and Angiogenesis during the Healing of Acetic Acid-Induced Gastric Ulcers in Rats
Cell proliferation and angiogenesis are of utmost importance for healing to take place. The KI67 and EGFR proteins are markers of cell proliferation, while CD31 and factor VIII are markers of angiogenesis. To elucidate the mechanism responsible for delayed healing of the gastric injury in old age, w...
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description | Cell proliferation and angiogenesis are of utmost importance for healing to take place. The KI67 and EGFR proteins are markers of cell proliferation, while CD31 and factor VIII are markers of angiogenesis. To elucidate the mechanism responsible for delayed healing of the gastric injury in old age, we analyzed the expression of these markers in rats of different months during the healing of an acetic acid-induced gastric ulcer. Male Wistar rats (aged 3, 6, 12, and 18 months) divided into four groups, according to their ages, formed the experimental animals. Stomach tissue samples were collected on days 3, 7, 14, and 21 after induction for assessment of ulcer healing. The area of gastric mucosa healed was inversely proportional to age. The expression of markers of proliferation (KI67 and EGFR) and angiogenesis (factor VIII and CD31) decreased significantly (p six months > 12 months > 18 months) on days 7, 14, and 21 after induction of gastric ulcer. This study revealed that the slower gastric ulcer healing rate in older rats might be due to reduced epithelial cell proliferation and angiogenic activities. |
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Folorunsho ; Olaleye, S. Babafemi</creator><contributor>Ulusoy, Mustafa Gurhan ; Mustafa Gurhan Ulusoy</contributor><creatorcontrib>Ajayi, A. Folorunsho ; Olaleye, S. Babafemi ; Ulusoy, Mustafa Gurhan ; Mustafa Gurhan Ulusoy</creatorcontrib><description>Cell proliferation and angiogenesis are of utmost importance for healing to take place. The KI67 and EGFR proteins are markers of cell proliferation, while CD31 and factor VIII are markers of angiogenesis. To elucidate the mechanism responsible for delayed healing of the gastric injury in old age, we analyzed the expression of these markers in rats of different months during the healing of an acetic acid-induced gastric ulcer. Male Wistar rats (aged 3, 6, 12, and 18 months) divided into four groups, according to their ages, formed the experimental animals. Stomach tissue samples were collected on days 3, 7, 14, and 21 after induction for assessment of ulcer healing. The area of gastric mucosa healed was inversely proportional to age. The expression of markers of proliferation (KI67 and EGFR) and angiogenesis (factor VIII and CD31) decreased significantly (p<0.05) in older rats when compared with younger ones (3 months > six months > 12 months > 18 months) on days 7, 14, and 21 after induction of gastric ulcer. This study revealed that the slower gastric ulcer healing rate in older rats might be due to reduced epithelial cell proliferation and angiogenic activities.</description><identifier>ISSN: 2356-6140</identifier><identifier>ISSN: 1537-744X</identifier><identifier>EISSN: 1537-744X</identifier><identifier>DOI: 10.1155/2020/3506207</identifier><identifier>PMID: 32549798</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Acetic Acid ; Acids ; Age ; Age Factors ; Aging ; Angiogenesis ; Animal tissues ; Animals ; Biomarkers - metabolism ; Blood coagulation factor VIII ; Cell growth ; Cell proliferation ; Cell Proliferation - physiology ; Coagulation factors ; Epidermal growth factor receptors ; Epithelial cells ; ErbB Receptors - biosynthesis ; Factor VIII - biosynthesis ; Gastric mucosa ; Growth factors ; Healing ; Immunohistochemistry - methods ; Injury analysis ; Ki-67 Antigen - biosynthesis ; Kinases ; Male ; Markers ; Neovascularization, Physiologic - physiology ; Organic acids ; Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis ; Potassium ; Proteins ; Rats, Wistar ; Stomach ; Stomach Ulcer - chemically induced ; Stomach Ulcer - metabolism ; Stomach Ulcer - physiopathology ; Ulcers ; Wound Healing - physiology</subject><ispartof>TheScientificWorld, 2020, Vol.2020 (2020), p.1-10</ispartof><rights>Copyright © 2020 A. Folorunsho Ajayi and S. Babafemi Olaleye.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 A. Folorunsho Ajayi and S. Babafemi Olaleye. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 A. Folorunsho Ajayi and S. 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Folorunsho</creatorcontrib><creatorcontrib>Olaleye, S. Babafemi</creatorcontrib><title>Immunohistochemical Studies of Age-Related Changes in Cell Proliferation and Angiogenesis during the Healing of Acetic Acid-Induced Gastric Ulcers in Rats</title><title>TheScientificWorld</title><addtitle>ScientificWorldJournal</addtitle><description>Cell proliferation and angiogenesis are of utmost importance for healing to take place. The KI67 and EGFR proteins are markers of cell proliferation, while CD31 and factor VIII are markers of angiogenesis. To elucidate the mechanism responsible for delayed healing of the gastric injury in old age, we analyzed the expression of these markers in rats of different months during the healing of an acetic acid-induced gastric ulcer. Male Wistar rats (aged 3, 6, 12, and 18 months) divided into four groups, according to their ages, formed the experimental animals. Stomach tissue samples were collected on days 3, 7, 14, and 21 after induction for assessment of ulcer healing. The area of gastric mucosa healed was inversely proportional to age. The expression of markers of proliferation (KI67 and EGFR) and angiogenesis (factor VIII and CD31) decreased significantly (p<0.05) in older rats when compared with younger ones (3 months > six months > 12 months > 18 months) on days 7, 14, and 21 after induction of gastric ulcer. This study revealed that the slower gastric ulcer healing rate in older rats might be due to reduced epithelial cell proliferation and angiogenic activities.</description><subject>Acetic Acid</subject><subject>Acids</subject><subject>Age</subject><subject>Age Factors</subject><subject>Aging</subject><subject>Angiogenesis</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Biomarkers - metabolism</subject><subject>Blood coagulation factor VIII</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - physiology</subject><subject>Coagulation factors</subject><subject>Epidermal growth factor receptors</subject><subject>Epithelial cells</subject><subject>ErbB Receptors - biosynthesis</subject><subject>Factor VIII - biosynthesis</subject><subject>Gastric mucosa</subject><subject>Growth factors</subject><subject>Healing</subject><subject>Immunohistochemistry - methods</subject><subject>Injury analysis</subject><subject>Ki-67 Antigen - biosynthesis</subject><subject>Kinases</subject><subject>Male</subject><subject>Markers</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Organic acids</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis</subject><subject>Potassium</subject><subject>Proteins</subject><subject>Rats, Wistar</subject><subject>Stomach</subject><subject>Stomach Ulcer - chemically induced</subject><subject>Stomach Ulcer - metabolism</subject><subject>Stomach Ulcer - physiopathology</subject><subject>Ulcers</subject><subject>Wound Healing - physiology</subject><issn>2356-6140</issn><issn>1537-744X</issn><issn>1537-744X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNks9rFDEUgAdR7Lp68ywDHnXa_JgkMxdhWbRdKCjVgreQSV5msswmNZlR_Ff8a81219aCB8nhhZcvH-_xXlG8xOgUY8bOCCLojDLECRKPigVmVFSirr8-LhaEMl5xXKOT4llKW4RoIzB7WpxQwupWtM2i-LXZ7WYfBpemoAfYOa3G8vM0GwepDLZc9VBdwagmMOV6UL7PaefLNYxj-SmG0VmIanLBl8qbcuV7F3rwkFwqzRyd78tpgPIC1Li_74UaJqdzcKbaeDPrLD5XaYo5eT1qiLf-KzWl58UTq8YEL45xWVx_eP9lfVFdfjzfrFeXlWa4zb12pm5p2zUN4lgw4IQhpFohEG8bA8jYTmgBVlnWAQdkTa0Zt9BhsJY0hC6LzcFrgtrKm-h2Kv6UQTl5mwixlyrmmkeQDa5FS0hHTdPVnSaKdx3ShnS2bTGYOrveHVw3c7cDo8FPUY0PpA9fvBtkH75LQRrc5Nkti9dHQQzfZkiT3IY5-ty_JDUmDWWUkHuqV7kq523IMr1zScsVp4QSzkWbqdN_UPmY_ZyDB-ty_sGHt4cPOoaUIti7wjGS-2WT-2WTx2XL-Ku_m72D_2xXBt4cgMF5o364_9RBZvK87mmCacMR_Q3LAOb7</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Ajayi, A. 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Folorunsho ; Olaleye, S. Babafemi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5197-7bd4939b8806175e62500a9770698de0dfb7c7efaf5be6e0fd4c56feb1eff2823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acetic Acid</topic><topic>Acids</topic><topic>Age</topic><topic>Age Factors</topic><topic>Aging</topic><topic>Angiogenesis</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Biomarkers - metabolism</topic><topic>Blood coagulation factor VIII</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - physiology</topic><topic>Coagulation factors</topic><topic>Epidermal growth factor receptors</topic><topic>Epithelial cells</topic><topic>ErbB Receptors - biosynthesis</topic><topic>Factor VIII - biosynthesis</topic><topic>Gastric mucosa</topic><topic>Growth factors</topic><topic>Healing</topic><topic>Immunohistochemistry - methods</topic><topic>Injury analysis</topic><topic>Ki-67 Antigen - biosynthesis</topic><topic>Kinases</topic><topic>Male</topic><topic>Markers</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Organic acids</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis</topic><topic>Potassium</topic><topic>Proteins</topic><topic>Rats, Wistar</topic><topic>Stomach</topic><topic>Stomach Ulcer - chemically induced</topic><topic>Stomach Ulcer - metabolism</topic><topic>Stomach Ulcer - physiopathology</topic><topic>Ulcers</topic><topic>Wound Healing - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ajayi, A. 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Folorunsho</au><au>Olaleye, S. Babafemi</au><au>Ulusoy, Mustafa Gurhan</au><au>Mustafa Gurhan Ulusoy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunohistochemical Studies of Age-Related Changes in Cell Proliferation and Angiogenesis during the Healing of Acetic Acid-Induced Gastric Ulcers in Rats</atitle><jtitle>TheScientificWorld</jtitle><addtitle>ScientificWorldJournal</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>2356-6140</issn><issn>1537-744X</issn><eissn>1537-744X</eissn><abstract>Cell proliferation and angiogenesis are of utmost importance for healing to take place. The KI67 and EGFR proteins are markers of cell proliferation, while CD31 and factor VIII are markers of angiogenesis. To elucidate the mechanism responsible for delayed healing of the gastric injury in old age, we analyzed the expression of these markers in rats of different months during the healing of an acetic acid-induced gastric ulcer. Male Wistar rats (aged 3, 6, 12, and 18 months) divided into four groups, according to their ages, formed the experimental animals. Stomach tissue samples were collected on days 3, 7, 14, and 21 after induction for assessment of ulcer healing. The area of gastric mucosa healed was inversely proportional to age. The expression of markers of proliferation (KI67 and EGFR) and angiogenesis (factor VIII and CD31) decreased significantly (p<0.05) in older rats when compared with younger ones (3 months > six months > 12 months > 18 months) on days 7, 14, and 21 after induction of gastric ulcer. 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subjects | Acetic Acid Acids Age Age Factors Aging Angiogenesis Animal tissues Animals Biomarkers - metabolism Blood coagulation factor VIII Cell growth Cell proliferation Cell Proliferation - physiology Coagulation factors Epidermal growth factor receptors Epithelial cells ErbB Receptors - biosynthesis Factor VIII - biosynthesis Gastric mucosa Growth factors Healing Immunohistochemistry - methods Injury analysis Ki-67 Antigen - biosynthesis Kinases Male Markers Neovascularization, Physiologic - physiology Organic acids Platelet Endothelial Cell Adhesion Molecule-1 - biosynthesis Potassium Proteins Rats, Wistar Stomach Stomach Ulcer - chemically induced Stomach Ulcer - metabolism Stomach Ulcer - physiopathology Ulcers Wound Healing - physiology |
title | Immunohistochemical Studies of Age-Related Changes in Cell Proliferation and Angiogenesis during the Healing of Acetic Acid-Induced Gastric Ulcers in Rats |
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