Expression Profiling Identifies <i>Klf15</i> as a Glucocorticoid Target That Regulates Airway Hyperresponsiveness

Masuno, Kiriko; Haldar, Saptarsi M.; Jeyaraj, Darwin; Mailloux, Christina M.; Huang, Xiaozhu; Panettieri, Rey A.; Jain, Mukesh K.; Gerber, Anthony N.

doi:10.1165/rcmb.2010-0369oc

Cited by 53 publications

(55 citation statements)

References 49 publications

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“…In cardiomyocytes, KLF15 cooperates with PPARα in regulating lipid metabolism (42). Conversely, activation of GR signaling can induce a number of KLFs (e.g., KLF9, KLF11, and KLF15) in specific physiologic or pathologic contexts (43)(44)(45). Finally, the current study illuminates the importance of cooperativity between KLFs and nuclear receptors at two levels: (a) direct cooperation with the ERR/PGC-1 module and (b) upstream regulation of PPARα.…”

Section: Methodsmentioning

confidence: 60%

Kruppel-like factor 4 is critical for transcriptional control of cardiac mitochondrial homeostasis

Liao

Zhang

Lü

et al. 2015

Journal of Clinical Investigation

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110

113

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Section: Methodsmentioning

confidence: 60%

Kruppel-like factor 4 is critical for transcriptional control of cardiac mitochondrial homeostasis

Liao

Zhang

Lü

et al. 2015

Journal of Clinical Investigation

Self Cite

110

113

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“…Klf15 is a direct target of the GR (32,(53)(54)(55). We found divergent epigenetic chromatin marks on the Klf15 GRE that paralleled the change in gene expression elicited by differential GC steroid dosing.…”

Section: Discussionmentioning

confidence: 74%

Intermittent glucocorticoid steroid dosing enhances muscle repair without eliciting muscle atrophy

Quattrocelli¹,

Barefield²,

Warner³

et al. 2017

Journal of Clinical Investigation

112

125

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“…KLF4 also stimulates the noncanonical Notch signaling pathway (71). KLF15 encodes a protein that interacts with a CG/TCCCC motif, G-rich motifs, or a CACCC site (59), and its expression is stimulated by glucocorticoids (52,80). KLF15 interacts with the Sp1 transcription factor (97) and, like most KLF factors, activates certain promoters while repressing others.…”

Section: Discussionmentioning

confidence: 99%

Cellular Transcription Factors Induced in Trigeminal Ganglia during Dexamethasone-Induced Reactivation from Latency Stimulate Bovine Herpesvirus 1 Productive Infection and Certain Viral Promoters

Workman

Eudy

Smith

et al. 2012

J Virol

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Bovine herpesvirus 1 (BHV-1), an alphaherpesvirinae subfamily member, establishes latency in sensory neurons. Elevated corticosteroid levels, due to stress, reproducibly triggers reactivation from latency in the field. A single intravenous injection of the synthetic corticosteroid dexamethasone (DEX) to latently infected calves consistently induces reactivation from latency. Lytic cycle viral gene expression is detected in sensory neurons within 6 h after DEX treatment of latently infected calves. These observations suggested that DEX stimulated expression of cellular genes leads to lytic cycle viral gene expression and productive infection. In this study, a commercially available assay-Bovine Gene Chip-was used to compare cellular gene expression in the trigeminal ganglia (TG) of calves latently infected with BHV-1 versus DEX-treated animals. Relative to TG prepared from latently infected calves, 11 cellular genes were induced more than 10-fold 3 h after DEX treatment. Pentraxin three, a regulator of innate immunity and neurodegeneration, was stimulated 35-to 63-fold after 3 or 6 h of DEX treatment. Two transcription factors, promyelocytic leukemia zinc finger (PLZF) and Slug were induced more than 15-fold 3 h after DEX treatment. PLZF or Slug stimulated productive infection 20-or 5-fold, respectively, and Slug stimulated the late glycoprotein C promoter more than 10-fold. Additional DEX-induced transcription factors also stimulated productive infection and certain viral promoters. These studies suggest that DEX-inducible cellular transcription factors and/or signaling pathways stimulate lytic cycle viral gene expression, which subsequently leads to successful reactivation from latency in a small subset of latently infected neurons. Bovine herpesvirus 1 (BHV-1) is an alphaherpesvirinae subfamily member that causes significant economical losses to the cattle industry (86). The ability of BHV-1 to suppress the immune system can result in life-threatening pneumonia due to secondary bacterial infections. This multifactorial disorder is referred to as bovine respiratory disease complex (reviewed in references 35 and 39). Like different alphaherpesvirinae subfamily members, the primary site for BHV-1 latency is sensory neurons within trigeminal ganglia (TG). Viral gene expression (73) and infectious virus (29) are detected in TG from 1 to 6 days after acute infection. Lytic cycle viral gene expression is subsequently extinguished in sensory neurons, and latency is established. The BHV-1 genome is stably maintained in sensory neurons, but infectious virus is not detected by standard virus isolation procedures (reviewed in references 33 and 34). The only viral gene abundantly expressed in latently infected sensory neurons is the latency-related (LR) gene (reviewed in reference 38). Stress, due to confinement, transporting cattle, restricting food and water, weaning, or increased corticosteroid levels increases the incidence of reactivation from latency (35, 39). The latency reactivation cycle of BHV-1 is crucial for vi...

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Expression Profiling Identifies Klf15 as a Glucocorticoid Target That Regulates Airway Hyperresponsiveness

Cited by 53 publications

References 49 publications

Kruppel-like factor 4 is critical for transcriptional control of cardiac mitochondrial homeostasis

Kruppel-like factor 4 is critical for transcriptional control of cardiac mitochondrial homeostasis

Intermittent glucocorticoid steroid dosing enhances muscle repair without eliciting muscle atrophy

Cellular Transcription Factors Induced in Trigeminal Ganglia during Dexamethasone-Induced Reactivation from Latency Stimulate Bovine Herpesvirus 1 Productive Infection and Certain Viral Promoters

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