Abstract
Background. Tumor necrosis factor alpha (TNFα) is implicated in a wide variety of pathological and physiological processes, including chronic inflammatory conditions, coronary artery disease, diabetes, obesity, and cachexia. Transgenic mice expressing human TNFα (hTNFα) have previously been described as a model for progressive rheumatoid arthritis. In this report, we describe extensive characterization of an hTNFα transgenic mouse line. Results. In addition to arthritis, these hTNFα transgenic mice demonstrated major alterations in body composition, metabolic rate, leptin levels, response to a high-fat diet, bone mineral density and content, impaired fertility and male sexual function. Many phenotypes displayed an earlier onset and a higher degree of severity in males, pointing towards a significant degree of sexual dimorphism in response to deregulated expression of TNFα. Conclusion. These results highlight the potential usefulness of this transgenic model as a resource for studying the progressive effects of constitutively expressed low levels of circulating TNFα, a condition mimicking that observed in a number of human pathological conditions.
| Original language | English |
|---|---|
| Article number | 13 |
| Journal | BMC Physiology |
| Volume | 7 |
| DOIs | |
| Publication status | Published - 2007 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
Cite this
An extensive phenotypic characterization of the hTNFα transgenic mice. / Hayward, Michael D.; Jones, Beverly K.; Saparov, Arman; Hain, Heather S.; Trillat, Anne Cecile; Bunzel, Michelle M.; Corona, Aaron; Li-Wang, Bifang; Strenkowski, Bryan; Giordano, Caroline; Shen, Hai; Arcamone, Emily; Weidlick, Jeffrey; Vilensky, Maria; Tugusheva, Marina; Felkner, Roland H.; Campbell, William; Rao, Yu; Grass, David S.; Buiakova, Olesia.
In: BMC Physiology, Vol. 7, 13, 2007.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - An extensive phenotypic characterization of the hTNFα transgenic mice
AU - Hayward, Michael D.
AU - Jones, Beverly K.
AU - Saparov, Arman
AU - Hain, Heather S.
AU - Trillat, Anne Cecile
AU - Bunzel, Michelle M.
AU - Corona, Aaron
AU - Li-Wang, Bifang
AU - Strenkowski, Bryan
AU - Giordano, Caroline
AU - Shen, Hai
AU - Arcamone, Emily
AU - Weidlick, Jeffrey
AU - Vilensky, Maria
AU - Tugusheva, Marina
AU - Felkner, Roland H.
AU - Campbell, William
AU - Rao, Yu
AU - Grass, David S.
AU - Buiakova, Olesia
PY - 2007
Y1 - 2007
N2 - Background. Tumor necrosis factor alpha (TNFα) is implicated in a wide variety of pathological and physiological processes, including chronic inflammatory conditions, coronary artery disease, diabetes, obesity, and cachexia. Transgenic mice expressing human TNFα (hTNFα) have previously been described as a model for progressive rheumatoid arthritis. In this report, we describe extensive characterization of an hTNFα transgenic mouse line. Results. In addition to arthritis, these hTNFα transgenic mice demonstrated major alterations in body composition, metabolic rate, leptin levels, response to a high-fat diet, bone mineral density and content, impaired fertility and male sexual function. Many phenotypes displayed an earlier onset and a higher degree of severity in males, pointing towards a significant degree of sexual dimorphism in response to deregulated expression of TNFα. Conclusion. These results highlight the potential usefulness of this transgenic model as a resource for studying the progressive effects of constitutively expressed low levels of circulating TNFα, a condition mimicking that observed in a number of human pathological conditions.
AB - Background. Tumor necrosis factor alpha (TNFα) is implicated in a wide variety of pathological and physiological processes, including chronic inflammatory conditions, coronary artery disease, diabetes, obesity, and cachexia. Transgenic mice expressing human TNFα (hTNFα) have previously been described as a model for progressive rheumatoid arthritis. In this report, we describe extensive characterization of an hTNFα transgenic mouse line. Results. In addition to arthritis, these hTNFα transgenic mice demonstrated major alterations in body composition, metabolic rate, leptin levels, response to a high-fat diet, bone mineral density and content, impaired fertility and male sexual function. Many phenotypes displayed an earlier onset and a higher degree of severity in males, pointing towards a significant degree of sexual dimorphism in response to deregulated expression of TNFα. Conclusion. These results highlight the potential usefulness of this transgenic model as a resource for studying the progressive effects of constitutively expressed low levels of circulating TNFα, a condition mimicking that observed in a number of human pathological conditions.
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UR - http://www.scopus.com/inward/citedby.url?scp=38849117807&partnerID=8YFLogxK
U2 - 10.1186/1472-6793-7-13
DO - 10.1186/1472-6793-7-13
M3 - Article
C2 - 18070349
AN - SCOPUS:38849117807
VL - 7
JO - BMC Physiology
JF - BMC Physiology
SN - 1472-6793
M1 - 13
ER -