Expression of aquaporins in intestine after heat stroke

Yuan-Hung Wang, Tsung-Ta Liu, Woon-Man Kung, Chun Chi Chen, Ya Ting Wen, I-Chan Lin, Chi Chang Huang, Li Wei

研究成果: 雜誌貢獻文章

8 引文 (Scopus)

摘要

Heat stroke (HS) has been shown to induce intestinal barrier dysfunction during whole body hyperthermia. HS-induced intestinal permeability change may result from modulation of aquaporin (AQP) expression, which subsequently regulates water homeostasis. This study aimed to evaluate AQP expression in the intestine of rats with HS at different recovery time points. Sprague-Dawley (SD) rats were exposed to an ambient temperature of 40 ± 0.5°C until a maximum core temperature of 40.5°C was attained. The small intestine was surgically removed and histologically examined, and AQP expression was determined by reverse transcription polymerase chain reaction and immunohistochemical staining. H&E staining revealed those intestinal villi were destroyed from HS0 to HS1 and rebuilt from HS3 to HS12. We further stain with activated caspase 3 found expressed at HS0 and back to normal at HS3. Investigation of AQP mRNA expression identified 10 genes. PCR results of AQP1, 3, 7, 8, and 11 transcripts were significantly higher in the HS group than in the sham group. Immunohistochemical staining showed a more than 11-fold increase in AQP3 and 11 expressions at HS0. AQP1 and 8 increased at HS1 and AQP7 increased at HS3 compared with those in the sham group. In this study, we found HS induced jejunum damage and cell apoptosis. AQPs were upregulation/downregulation after HS in different time point suggested that water/glycerol transport was important when hyperthermia occurred. Furthermore, the biological function of the AQP needs more exploration in response to HS.
原文英語
頁(從 - 到)8742-53
頁數12
期刊International Journal of Clinical and Experimental Pathology
8
發行號8
出版狀態已發佈 - 2015

指紋

Heat Stroke
Aquaporins
Intestines
Staining and Labeling
Fever
Polymerase Chain Reaction
Temperature
Water
Jejunum
Caspase 3
Glycerol
Reverse Transcription
Small Intestine
Sprague Dawley Rats
Permeability
Homeostasis
Coloring Agents
Up-Regulation
Down-Regulation
Apoptosis

引用此文

Expression of aquaporins in intestine after heat stroke. / Wang, Yuan-Hung; Liu, Tsung-Ta; Kung, Woon-Man; Chen, Chun Chi; Wen, Ya Ting; Lin, I-Chan; Huang, Chi Chang; Wei, Li.

於: International Journal of Clinical and Experimental Pathology, 卷 8, 編號 8, 2015, p. 8742-53.

研究成果: 雜誌貢獻文章

Wang, Y-H, Liu, T-T, Kung, W-M, Chen, CC, Wen, YT, Lin, I-C, Huang, CC & Wei, L 2015, 'Expression of aquaporins in intestine after heat stroke', International Journal of Clinical and Experimental Pathology, 卷 8, 編號 8, 頁 8742-53.
Wang, Yuan-Hung ; Liu, Tsung-Ta ; Kung, Woon-Man ; Chen, Chun Chi ; Wen, Ya Ting ; Lin, I-Chan ; Huang, Chi Chang ; Wei, Li. / Expression of aquaporins in intestine after heat stroke. 於: International Journal of Clinical and Experimental Pathology. 2015 ; 卷 8, 編號 8. 頁 8742-53.
@article{633a2803b5d84ea684e8eab3dbc6c950,
title = "Expression of aquaporins in intestine after heat stroke",
abstract = "Heat stroke (HS) has been shown to induce intestinal barrier dysfunction during whole body hyperthermia. HS-induced intestinal permeability change may result from modulation of aquaporin (AQP) expression, which subsequently regulates water homeostasis. This study aimed to evaluate AQP expression in the intestine of rats with HS at different recovery time points. Sprague-Dawley (SD) rats were exposed to an ambient temperature of 40 ± 0.5°C until a maximum core temperature of 40.5°C was attained. The small intestine was surgically removed and histologically examined, and AQP expression was determined by reverse transcription polymerase chain reaction and immunohistochemical staining. H&E staining revealed those intestinal villi were destroyed from HS0 to HS1 and rebuilt from HS3 to HS12. We further stain with activated caspase 3 found expressed at HS0 and back to normal at HS3. Investigation of AQP mRNA expression identified 10 genes. PCR results of AQP1, 3, 7, 8, and 11 transcripts were significantly higher in the HS group than in the sham group. Immunohistochemical staining showed a more than 11-fold increase in AQP3 and 11 expressions at HS0. AQP1 and 8 increased at HS1 and AQP7 increased at HS3 compared with those in the sham group. In this study, we found HS induced jejunum damage and cell apoptosis. AQPs were upregulation/downregulation after HS in different time point suggested that water/glycerol transport was important when hyperthermia occurred. Furthermore, the biological function of the AQP needs more exploration in response to HS.",
keywords = "Journal Article, Research Support, Non-U.S. Gov't",
author = "Yuan-Hung Wang and Tsung-Ta Liu and Woon-Man Kung and Chen, {Chun Chi} and Wen, {Ya Ting} and I-Chan Lin and Huang, {Chi Chang} and Li Wei",
year = "2015",
language = "English",
volume = "8",
pages = "8742--53",
journal = "International Journal of Clinical and Experimental Pathology",
issn = "1936-2625",
publisher = "E-CENTURY PUBLISHING CORP",
number = "8",

}

TY - JOUR

T1 - Expression of aquaporins in intestine after heat stroke

AU - Wang, Yuan-Hung

AU - Liu, Tsung-Ta

AU - Kung, Woon-Man

AU - Chen, Chun Chi

AU - Wen, Ya Ting

AU - Lin, I-Chan

AU - Huang, Chi Chang

AU - Wei, Li

PY - 2015

Y1 - 2015

N2 - Heat stroke (HS) has been shown to induce intestinal barrier dysfunction during whole body hyperthermia. HS-induced intestinal permeability change may result from modulation of aquaporin (AQP) expression, which subsequently regulates water homeostasis. This study aimed to evaluate AQP expression in the intestine of rats with HS at different recovery time points. Sprague-Dawley (SD) rats were exposed to an ambient temperature of 40 ± 0.5°C until a maximum core temperature of 40.5°C was attained. The small intestine was surgically removed and histologically examined, and AQP expression was determined by reverse transcription polymerase chain reaction and immunohistochemical staining. H&E staining revealed those intestinal villi were destroyed from HS0 to HS1 and rebuilt from HS3 to HS12. We further stain with activated caspase 3 found expressed at HS0 and back to normal at HS3. Investigation of AQP mRNA expression identified 10 genes. PCR results of AQP1, 3, 7, 8, and 11 transcripts were significantly higher in the HS group than in the sham group. Immunohistochemical staining showed a more than 11-fold increase in AQP3 and 11 expressions at HS0. AQP1 and 8 increased at HS1 and AQP7 increased at HS3 compared with those in the sham group. In this study, we found HS induced jejunum damage and cell apoptosis. AQPs were upregulation/downregulation after HS in different time point suggested that water/glycerol transport was important when hyperthermia occurred. Furthermore, the biological function of the AQP needs more exploration in response to HS.

AB - Heat stroke (HS) has been shown to induce intestinal barrier dysfunction during whole body hyperthermia. HS-induced intestinal permeability change may result from modulation of aquaporin (AQP) expression, which subsequently regulates water homeostasis. This study aimed to evaluate AQP expression in the intestine of rats with HS at different recovery time points. Sprague-Dawley (SD) rats were exposed to an ambient temperature of 40 ± 0.5°C until a maximum core temperature of 40.5°C was attained. The small intestine was surgically removed and histologically examined, and AQP expression was determined by reverse transcription polymerase chain reaction and immunohistochemical staining. H&E staining revealed those intestinal villi were destroyed from HS0 to HS1 and rebuilt from HS3 to HS12. We further stain with activated caspase 3 found expressed at HS0 and back to normal at HS3. Investigation of AQP mRNA expression identified 10 genes. PCR results of AQP1, 3, 7, 8, and 11 transcripts were significantly higher in the HS group than in the sham group. Immunohistochemical staining showed a more than 11-fold increase in AQP3 and 11 expressions at HS0. AQP1 and 8 increased at HS1 and AQP7 increased at HS3 compared with those in the sham group. In this study, we found HS induced jejunum damage and cell apoptosis. AQPs were upregulation/downregulation after HS in different time point suggested that water/glycerol transport was important when hyperthermia occurred. Furthermore, the biological function of the AQP needs more exploration in response to HS.

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85012965405&origin=resultslist&sort=plf-f&src=s&st1=Expression+of+aquaporins+in+intestine+after+heat+stroke&st2=&sid=89d9328e30aa577107132d41e3cbba39&sot=b&sdt=b&sl=70&s=TITLE-ABS-KEY%28Expression+of+aquaporins+in+intestine+after+heat+stroke%29&relpos=0&citeCnt=3&searchTerm=

UR - https://www.scopus.com/results/citedbyresults.uri?sort=plf-f&cite=2-s2.0-85012965405&src=s&imp=t&sid=6303252813448bd43cd56e86df6e629e&sot=cite&sdt=a&sl=0&origin=recordpage&editSaveSearch=&txGid=20060b07e9d75767a005796580f20820

M3 - Article

C2 - 26464618

VL - 8

SP - 8742

EP - 8753

JO - International Journal of Clinical and Experimental Pathology

JF - International Journal of Clinical and Experimental Pathology

SN - 1936-2625

IS - 8

ER -