Novel therapy for myocardial infarction: can HGF/Met be beneficial?

Sala, Valentina; Crepaldi, Tiziana

doi:10.1007/s00018-011-0633-6

Cited by 37 publications

(24 citation statements)

References 169 publications

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“…In a mouse model, TLR2 activation of neutrophils led to the release of MMP9, which was protective against experimentally-induced asthma [57]. HGF has been proposed as a modulator of cardiac tissue repair [58]. The expression of HGF and its secretion into the blood circulation are promoted during the early phase of myocardial infarction [59].…”

Section: Discussionmentioning

confidence: 99%

Genomic Responses during Acute Human Anaphylaxis Are Characterized by Upregulation of Innate Inflammatory Gene Networks

et al. 2014

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BackgroundSystemic spread of immune activation and mediator release is required for the development of anaphylaxis in humans. We hypothesized that peripheral blood leukocyte (PBL) activation plays a key role.ObjectiveTo characterize PBL genomic responses during acute anaphylaxis.MethodsPBL samples were collected at three timepoints from six patients presenting to the Emergency Department (ED) with acute anaphylaxis and six healthy controls. Gene expression patterns were profiled on microarrays, differentially expressed genes were identified, and network analysis was employed to explore underlying mechanisms.ResultsPatients presented with moderately severe anaphylaxis after oral aspirin (2), peanut (2), bee sting (1) and unknown cause (1). Two genes were differentially expressed in patients compared to controls at ED arrival, 67 genes at 1 hour post-arrival and 2,801 genes at 3 hours post-arrival. Network analysis demonstrated that three inflammatory modules were upregulated during anaphylaxis. Notably, these modules contained multiple hub genes, which are known to play a central role in the regulation of innate inflammatory responses. Bioinformatics analyses showed that the data were enriched for LPS-like and TNF activation signatures.ConclusionPBL genomic responses during human anaphylaxis are characterized by dynamic expression of innate inflammatory modules. Upregulation of these modules was observed in patients with different reaction triggers. Our findings indicate a role for innate immune pathways in the pathogenesis of human anaphylaxis, and the hub genes identified in this study represent logical candidates for follow-up studies.

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Section: Discussionmentioning

confidence: 99%

Genomic Responses during Acute Human Anaphylaxis Are Characterized by Upregulation of Innate Inflammatory Gene Networks

et al. 2014

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“…Several pathological conditions, including tumor growth, ischemia/reperfusion, diabetes, rheumatoid arthritis, atherosclerosis, and inflammatory processes also require neoangiogenesis. It is therefore not surprising that angiogenesis is therapeutically targeted in several human disorders (4,5).…”

mentioning

confidence: 99%

Role of c-Met/Phosphatidylinositol 3-Kinase (PI3k)/Akt Signaling in Hepatocyte Growth Factor (HGF)-mediated Lamellipodia Formation, Reactive Oxygen Species (ROS) Generation, and Motility of Lung Endothelial Cells

Usatyuk

Mohan

et al. 2014

Journal of Biological Chemistry

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Background: Lamellipodia structures provide a platform for the spatio-temporal localization of key components necessary for cell migration. Results: HGF activates c-Met/PI3k/Akt signaling axis, which is essential for the recruitment of actin, cortactin, p47phox , and Rac1and ROS production in lamellipodia. Conclusion: HGF-induced spatio-temporal localization of cytoskeletal proteins and NADPH oxidase components regulate lamellipodial ROS and cell migration. Significance: This study identifies a novel role for lamellipodial ROS in cell motility.

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“…HGF has a cardioprotective role in experimentally induced myocardial infarction, preventing cardiomyocyte apoptosis, inducing angiogenesis, and improving impaired heart function (Aoki et al, 2000; Jayasankar et al, 2003; Sala and Crepaldi, 2011). …”

Section: Hgf and Igf1 In Cardiac Stem Cellsmentioning

confidence: 99%

Targeting pleiotropic signaling pathways to control adult cardiac stem cell fate and function

et al. 2014

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The identification of different pools of cardiac progenitor cells resident in the adult mammalian heart opened a new era in heart regeneration as a means to restore the loss of functional cardiac tissue and overcome the limited availability of donor organs. Indeed, resident stem cells are believed to participate to tissue homeostasis and renewal in healthy and damaged myocardium although their actual contribution to these processes remain unclear. The poor outcome in terms of cardiac regeneration following tissue damage point out at the need for a deeper understanding of the molecular mechanisms controlling CPC behavior and fate determination before new therapeutic strategies can be developed. The regulation of cardiac resident stem cell fate and function is likely to result from the interplay between pleiotropic signaling pathways as well as tissue- and cell-specific regulators. Such a modular interaction—which has already been described in the nucleus of a number of different cells where transcriptional complexes form to activate specific gene programs—would account for the unique responses of cardiac progenitors to general and tissue-specific stimuli. The study of the molecular determinants involved in cardiac stem/progenitor cell regulatory mechanisms may shed light on the processes of cardiac homeostasis in health and disease and thus provide clues on the actual feasibility of cardiac cell therapy through tissue-specific progenitors.

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Novel therapy for myocardial infarction: can HGF/Met be beneficial?

Cited by 37 publications

References 169 publications

Genomic Responses during Acute Human Anaphylaxis Are Characterized by Upregulation of Innate Inflammatory Gene Networks

Genomic Responses during Acute Human Anaphylaxis Are Characterized by Upregulation of Innate Inflammatory Gene Networks

Role of c-Met/Phosphatidylinositol 3-Kinase (PI3k)/Akt Signaling in Hepatocyte Growth Factor (HGF)-mediated Lamellipodia Formation, Reactive Oxygen Species (ROS) Generation, and Motility of Lung Endothelial Cells

Targeting pleiotropic signaling pathways to control adult cardiac stem cell fate and function

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