Hypoxia: jump-starting inflammation

Melillo, Giovanni

doi:10.1182/blood-2010-12-324913

Cited by 17 publications

(8 citation statements)

References 11 publications

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“…In addition to TREM‐1, HIF‐1α may be a therapeutic target of psoriasis (Rosenberger et al, ). In the present study, we found that LPS stimulated HIF‐1α accumulation in HaCaT cells, which is consistent with previous studies on macrophages and dendritic cells (Blouin et al, ; Melillo, ). Thus, bacterial infection may activate HIF‐1α expression in keratinocytes, which may be involved in the initiation of psoriasis.…”

Section: Discussionsupporting

confidence: 93%

Lipopolysaccharide induces TREM‐1‐dependent HIF‐1α expression in human keratinocyte cell line

Wang

Xiao

et al. 2016

Cell Biology International

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Bacterial infection is an important factor that can trigger and exacerbate psoriasis. The protein triggering receptor expressed on myeloid cells type-1 (TREM-1) is overexpressed in psoriasis and decreased after a successful treatment. Hypoxia inducible factor-1α (HIF-1α), subunit of the transcription factor HIF-1, has participated in angiogenesis and inflammation in psoriasis. Increased expressions of TREM-1 and HIF-1α are associated with the infection of microbial pathogens. However, the association between TREM-1 and HIF-1α still needs to be elucidated. Results of immunofluorescence showed an overexpression of TREM-1 and HIF-1α in HaCaT keratinocytes exposed to 1 µg/mL of lipopolysaccharide (LPS). Particularly, silencing of TREM-1 expression by siRNA suppressed the inducible effect of LPS on phosphoinositide 3-kinase (PI3 K)/Akt, the critical transduction mediator, and HIF-1α. Furthermore, the PI3 K inhibitor wortmannin effectively blocked the increased level of HIF-1α induced by LPS. However, there was no significant change in LPS-induced expression of TREM-1. Expressions of TREM-1, HIF-1α, and phosphorylated Akt proteins were further examined by real-time PCR and Western blot, respectively. Our data suggest that TREM-1 and HIF-1α are expressed on keratinocytes and could be upregulated by bacterial infection. Moreover, LPS-induced TREM-1 has an ability to mediate the expression of HIF-1α in HaCaT cells through the PI3 K/Akt pathway. Our study provides new insights into the possible mechanism of TREM-1 and HIF-1α in psoriasis.

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Section: Discussionsupporting

confidence: 93%

Lipopolysaccharide induces TREM‐1‐dependent HIF‐1α expression in human keratinocyte cell line

Wang

Xiao

et al. 2016

Cell Biology International

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“…The regulation of VEGF and its biological actions replicate this co-dependence on the molecular level. VEGF expression is induced by hypoxia, a frequent condition in inflammatory lesions [53]. The proinflammatory cytokines interleukin-1ß, tumor necrosis factor-alpha and interleukin-18 [54,55] directly promote VEGF production in various cells types.…”

Section: The Molecular Basis: Vascular Mediators In Autoimmune Demyelmentioning

confidence: 99%

Vascular pathology in multiple sclerosis: mind boosting or myth busting?

Waschbisch

Manzel

Linker

et al. 2011

Exp & Trans Stroke Med

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The investigation of central nervous system vascular changes in the pathophysiology of multiple sclerosis (MS) is a time-honored concept. Yet, recent reports on changes in venous cerebrospinal outflow, the advent of new magnetic resonance imaging techniques and the investigation of immunomodulatory properties of several vascular mediators on the molecular level have added new excitement to hypotheses centering around vascular pathology as determining factor in the pathophysiology of MS. Here we critically review the concept of chronic cerebrospinal venous insufficiency in MS patients and describe new imaging techniques including perfusion weighted imaging, susceptibility weighted imaging and diffusion weighted imaging which reveal central nervous system hypoperfusion, perivascular iron deposition and diffuse structural changes in the MS brain. On a molecular basis, vascular mediators represent interesting targets connecting vascular pathology with immunomodulation. In summary, the relation of venous changes to the pathophysiology of MS may not be as simple as initially described and it certainly seems awkward to think of the complex disease MS solely as result of a simple venous outflow obstruction. Yet, the investigation of new vascular concepts as one variable in the pathophysiology of the autoimmune attack seems very worthwhile and may add to a better understanding of this devastating disorder.

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“…Some studies claim that hypoxia recruits inflammatory cells of innate and adaptive immunity and exacerbates the inflammatory process; this sensitive response is mediated by HIF‐1α that operates a complex inflammatory response in microenvironments, playing an important role in renal pathogenesis. Yu et al recruited 32 patients with a diagnosis of postgraft CKD, with microcirculation impairment among inflammatory renal cell infiltrates.…”

Section: Discussionmentioning

confidence: 99%

Role of hypoxia‐inducible factor 1α as a potential biomarker for renal diseases—A systematic review

Encinas

Foncesca

Perez

et al. 2019

Cell Biochemistry & Function

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Renal cells need oxygen for homeostasis; it is known for adjusting cellular functioning and the energy obtainment have a broad relationship with cellular respiration, through the O2 bioavailability. O2 homeostasis regulation in the kidney is mediated by hypoxia‐inducible factors (HIFs). HIF is divided into three α isoforms, represented by HIF‐1α, HIF‐2α, and HIF‐3α in addition to three paralogs of HIF‐1β; these are involved in some metabolic processes, as well as in the pathogenesis of several diseases. Renal biopsy analyses of patients and experimental animal models aim to understand the relationship between HIF and protection against developing renal diseases or the induction of their onset, being thus this molecule can be considered a potential biomarker of renal disease. We carried out a systematic review to which we included studies on HIF‐1α and renal disease in the last 5 years (2013‐2018) in researches with humans and/or animal model through searches in three databases: LILACS, PubMed, and SciELO by two researchers. We obtained 22 articles that discussed the relationship with HIF as inductor or protector against renal disease and no relation between HIF and renal. We observed controversies remain regarding the relation between of HIF with renal diseases; this may be related to the different intracellular pathways mediated by HIF‐1α, thereby determining differentiated cellular responses.

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Hypoxia: jump-starting inflammation

Cited by 17 publications

References 11 publications

Lipopolysaccharide induces TREM‐1‐dependent HIF‐1α expression in human keratinocyte cell line

Lipopolysaccharide induces TREM‐1‐dependent HIF‐1α expression in human keratinocyte cell line

Vascular pathology in multiple sclerosis: mind boosting or myth busting?

Role of hypoxia‐inducible factor 1α as a potential biomarker for renal diseases—A systematic review

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