Notch signaling regulates expression of Mcl-1 and apoptosis in PPD-treated macrophages

Palaga, Tanapat; Ratanabunyong, Siriluk; Pattarakankul, Thitiporn; Sangphech, Naunpun; Wongchana, Wipawee; Hadae, Yukihiro; Kueanjinda, Patipark

doi:10.1038/cmi.2013.22

Cited by 32 publications

(29 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This is not surprising because NOTCH, being a transcription factor, may stimulate its own expression. Consistent with this notion, increased expression of NOTCH1 protein was observed following NOTCH1 activation by Mycobacterium bovis in macrophages 37. These observations suggest that NOTCH3, but not NOTCH1, may contribute to RV-induced GCH in COPD.…”

Section: Discussionsupporting

confidence: 69%

NOTCH3 contributes to rhinovirus-induced goblet cell hyperplasia in COPD airway epithelial cells

Jing

Gimenes-Júnior

Mishra

et al. 2018

Thorax

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 69%

NOTCH3 contributes to rhinovirus-induced goblet cell hyperplasia in COPD airway epithelial cells

Jing

Gimenes-Júnior

Mishra

et al. 2018

Thorax

View full text Add to dashboard Cite

show abstract

“…Phosphorylation of the IκB is extremely responsible for dissociation of the inactive NF-κB dimers, which makes the latter translocate into the nucleus and binds to the IL-6 DNA (47). Furthermore, Palaga et al confirmed that NF-κB directly involves in the positive regulation IL-6 gene by Notch1 signal in activated macrophages (48). …”

Section: Nuclear Factor-κbmentioning

confidence: 96%

Hall of Fame among Pro-inflammatory Cytokines: Interleukin-6 Gene and Its Transcriptional Regulation Mechanisms

2016

View full text Add to dashboard Cite

Pro-inflammatory cytokines that are generated by immune system cells and mediate many kinds of immune responses are kinds of endogenous polypeptides. They are also the effectors of the autoimmune system. It is generally accepted that interleukin (IL)-4, IL-6, IL-9, IL-17, and tumor necrosis factor-α are pro-inflammatory cytokines; however, IL-6 becomes a protagonist among them since it predominately induces pro-inflammatory signaling and regulates massive cellular processes. It has been ascertained that IL-6 is associated with a large number of diseases with inflammatory background, such as anemia of chronic diseases, angiogenesis acute-phase response, bone metabolism, cartilage metabolism, and multiple cancers. Despite great progress in the relative field, the targeted regulation of IL-6 response for therapeutic benefits remains incompletely to be understood. Therefore, it is conceivable that understanding mechanisms of IL-6 from the perspective of gene regulation can better facilitate to determine the pathogenesis of the disease, providing more solid scientific basis for clinical treatment translation. In this review, we summarize the candidate genes that have been implicated in clinical target therapy from the perspective of gene transcription regulation.

show abstract

“…Studies comparing BCG with M. tuberculosis have frequently used high Multiplicity-of-Infection (MOI). In general, studies use BCG infection at MOI 10 (10 bacilli/cell) pointing apoptosis as a cellular strategy to eliminate mycobacteria [20, 21]. …”

Section: Introductionmentioning

confidence: 99%

Low Dose BCG Infection as a Model for Macrophage Activation Maintaining Cell Viability

Chávez‐Galán

Vesin

Martinvalet

et al. 2016

Journal of Immunology Research

View full text Add to dashboard Cite

Mycobacterium bovis BCG, the current vaccine against tuberculosis, is ingested by macrophages promoting the development of effector functions including cell death and microbicidal mechanisms. Despite accumulating reports on M. tuberculosis, mechanisms of BCG/macrophage interaction remain relatively undefined. In vivo, few bacilli are sufficient to establish a mycobacterial infection; however, in vitro studies systematically use high mycobacterium doses. In this study, we analyze macrophage/BCG interactions and microenvironment upon infection with low BCG doses and propose an in vitro model to study cell activation without affecting viability. We show that RAW macrophages infected with BCG at MOI 1 activated higher and sustained levels of proinflammatory cytokines and transcription factors while MOI 0.1 was more efficient for early stimulation of IL-1β, MCP-1, and KC. Both BCG infection doses induced iNOS and NO in a dose-dependent manner and maintained nuclear and mitochondrial structures. Microenvironment generated by MOI 1 induced macrophage proliferation but not MOI 0.1 infection. In conclusion, BCG infection at low dose is an efficient in vitro model to study macrophage/BCG interactions that maintains macrophage viability and mitochondrial structures. This represents a novel model that can be applied to BCG research fields including mycobacterial infections, cancer immunotherapy, and prevention of autoimmunity and allergies.

show abstract

Notch signaling regulates expression of Mcl-1 and apoptosis in PPD-treated macrophages

Cited by 32 publications

References 41 publications

NOTCH3 contributes to rhinovirus-induced goblet cell hyperplasia in COPD airway epithelial cells

NOTCH3 contributes to rhinovirus-induced goblet cell hyperplasia in COPD airway epithelial cells

Hall of Fame among Pro-inflammatory Cytokines: Interleukin-6 Gene and Its Transcriptional Regulation Mechanisms

Low Dose BCG Infection as a Model for Macrophage Activation Maintaining Cell Viability

Contact Info

Product

Resources

About