Microarray study of genes differentially modulated in response to nitric oxide in macrophages

Nan, Xuehua; Maeng, Oky; Shin, Hyo Jung; An, Hyun‐Jung; Yeom, Young‐Il; Lee, Hayyoung; Paik, Sang‐Gi

doi:10.1080/19768354.2008.9647149

Animal Cells and Systems

2008

DOI: 10.1080/19768354.2008.9647149

|View full text |Cite

Microarray study of genes differentially modulated in response to nitric oxide in macrophages

Xuehua Nan

Oky Maeng

Hyo Jung Shin

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2011

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

The survival effect of mitochondrial Higd-1a is associated with suppression of cytochrome C release and prevention of caspase activation

Shin

et al. 2011

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

View full text Add to dashboard Cite

Higd-1a (hypoxia induced gene domain family-1a) is a mitochondrial inner membrane protein with a conformation of N-terminal outside-C-terminal outside and loop inside. There are four Higd genes, Higd-1a, -1b, -1c and -2a, in the mouse. Higd-1a and -2a are expressed primarily in the brain, heart, kidney and leukocytes. HIF (hypoxia-inducible factor) overexpression induced the endogenous expression and promoter activity of Higd-1a. Mutation of the HRE (hypoxia-response element) site at -32bp in the Higd-1a promoter reduced the promoter activity, suggesting that transcription of Higd-1a is regulated by binding of the transcription factor HIF to the HRE. Higd-1a promoted cell survival under hypoxia. RAW264.7 cells stably transfected with Higd-1a underwent less apoptosis than control cells in a hypoxic condition, and hypoxia-induced apoptosis was strongly enhanced when endogenous Higd-1a was silenced by siRNA. The survival effect of Higd-1a was completely abolished by deletion of the 26 N-terminal amino acids, and we showed that Higd-1a increased survival by inhibiting cytochrome C release and reducing the activities of caspases. However, expression of Bcl-2, Bax, Bad, and BNIP3 and translocation of AIF were unaffected under the same conditions. Higd-2a also enhanced cell survival under hypoxia. Cells transfected with Higd-2a underwent less apoptosis than control cells in hypoxic conditions, and hypoxia-induced apoptosis increased when endogenous Higd-2a was depleted. Together these observations indicate that Higd-1a is induced by hypoxia in a HIF-dependent manner and its anti-apoptotic effect results from inhibiting cytochrome C release and reducing caspase activities.

show abstract

The survival effect of mitochondrial Higd-1a is associated with suppression of cytochrome C release and prevention of caspase activation

Shin

et al. 2011

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Microarray study of genes differentially modulated in response to nitric oxide in macrophages

Cited by 1 publication

References 19 publications

The survival effect of mitochondrial Higd-1a is associated with suppression of cytochrome C release and prevention of caspase activation

The survival effect of mitochondrial Higd-1a is associated with suppression of cytochrome C release and prevention of caspase activation

Contact Info

Product

Resources

About