Deficiency of IL-12p35 improves cardiac repair after myocardial infarction by promoting angiogenesis

Kan, Xiaoyu; Ma, Youcai; Zhang, Congcong; Li, Ping; Li-ping, WU; Zhang, Shuai; Li, Yulin; Du, Jie

doi:10.1093/cvr/cvv255

Cited by 41 publications

(41 citation statements)

References 47 publications

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“…Just as Table 4. Although IL-12 family Fairweather et al, 2003;Yang et al, 2011;Nyland et al, 2012;Jenke et al, 2014;Kong et al, 2014;Hu et al, 2014;Zha et al, 2015;Zhang et al, 2017;Miteva et al, 2017;Sesti-Costa et al, 2017;Ouyang et al, 2017;Xu et al, 2018 Zhou et al, 2001;Kempe et al, 2009;Correia et al, 2010;Lin et al, 2012;Khojasteh-Fard et al, 2012;Jin et al, 2012;Yong et al, 2013;Chistiakov et al, 2015;Abbas et al, 2015;A Shahi et al, 2015;Zykov et al, 2016;Opstad et al, 2016;Zhu et al, 2018;Rasa et al, 2018; Lee et al, 1999;Davenport and Tipping, 2003;Hauer et al, 2005;Koltsova et al, 2012;Hirase et al, 2013;Subramanian et al, 2015;Kan et al, 2016;Tao et al, 2016;Engelbertsen et al, 2018;Fatkhullina et al, 2018;Ryu et al, 2018;Huang et al, 2019;Huang et al, 2019;Wang et al, 2019;Jia et...…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating animal study reports also demonstrate that treatment with exogenous recombinant murine IL-12 significantly aggravates the progression of atherosclerosis, and increases aortic atherosclerotic plaque areas in both ApoEknockout mice and in low density lipoprotein (LDL) receptordeficient mice, while cancelation the biological effects of IL-12 can significantly diminish such effects (Lee et al, 1999;Davenport and Tipping, 2003;Hauer et al, 2005). In a murine myocardial infarction model, canceling the biological effects of IL-12 alleviates cardiac dysfunction by promoting angiogenesis (Kan et al, 2016). In a recent study, Shi et al reported that knockout of IL-12p35 subunit, which can cancel the biological effects of IL-12 and IL-35, significantly aggravated Th1/Th2 and Th17/Treg imbalance and increased atherosclerotic plaque areas in ApoE mice, which may suggest that the pro-atherosclerotic effects of IL-12 can be mediated by promoting the CD4+ T lymphocyte differentiation imbalance .…”

Section: Animal Studiesmentioning

confidence: 99%

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Roles and Mechanisms of Interleukin-12 Family Members in Cardiovascular Diseases: Opportunities and Challenges

Wang

et al. 2020

Front. Pharmacol.

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Cardiovascular diseases represent a complex group of clinical syndromes caused by a variety of interacting pathological factors. They include the most extensive disease population and rank first in all-cause mortality worldwide. Accumulating evidence demonstrates that cytokines play critical roles in the presence and development of cardiovascular diseases. Interleukin-12 family members, including IL-12, IL-23, IL-27 and IL-35, are a class of cytokines that regulate a variety of biological effects; they are closely related to the progression of various cardiovascular diseases, including atherosclerosis, hypertension, aortic dissection, cardiac hypertrophy, myocardial infarction, and acute cardiac injury. This paper mainly discusses the role of IL-12 family members in cardiovascular diseases, and the molecular and cellular mechanisms potentially involved in their action in order to identify possible intervention targets for the prevention and clinical treatment of cardiovascular diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Animal Studiesmentioning

confidence: 99%

Roles and Mechanisms of Interleukin-12 Family Members in Cardiovascular Diseases: Opportunities and Challenges

Wang

et al. 2020

Front. Pharmacol.

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“…On the other hand, the predominance of non-inflammatory monocytes could potentially lead to a better outcome, due to the capacity of this population to enter the damaged tissues in a CX3CR1-mediated manner to repair tissue damage, secrete anti-inflammatory cytokines, and promote regeneration [ 14 , 16 ]. This positive effect has been demonstrated in myocardial infarction, where non-inflammatory patrolling monocytes enter the cardiac muscle to recover damage and promote angiogenesis [ 53 , 54 ]. Non-inflammatory monocytes also act in neurodegenerative diseases like Alzheimer’s disease, where they remove amyloid-β peptides from the brain vasculature [ 55 ], and are also known to prevent excitotoxicity [ 56 ], which could also explain the positive correlation found with survival, as glutamate-induced excitotoxicity is one of the pathological mechanisms found to participate in ALS pathogeny.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory and non-inflammatory monocytes as novel prognostic biomarkers of survival in SOD1G93A mouse model of Amyotrophic Lateral Sclerosis

et al. 2017

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Amyotrophic Lateral Sclerosis (ALS) has lately become a suitable scenario to study the interplay between the hematopoietic system and disease progression. Recent studies in C9orf72 null mice have demonstrated that C9orf72 is necessary for the normal function of myeloid cells. In this study, we aimed to analyze in depth the connection between the hematopoietic system and secondary lymphoid (spleen) and non-lymphoid (liver and skeletal muscle) organs and tissues along the disease progression in the transgenic SOD1G93A mice. Our findings suggested that the inflammatory response due to the neurodegeneration in this animal model affected all three organs and tissues, especially the liver and the skeletal muscle. However, the liver was able to compensate this inflammatory response by means of the action of non-inflammatory monocytes, while in the skeletal muscle inflammatory monocytes prompted a further inflammation process until the terminal state of the animals. Interestingly, in blood, a positive correlation was found between non-inflammatory monocytes and survival of the transgenic SOD1G93A mice, while the contrary (a negative correlation) was found in the case of inflammatory monocytes, supporting their potential role as biomarkers of disease progression and survival in this animal model. These findings could prompt future translational studies in ALS patients, promoting the identification of new reliable biomarkers of disease progression.

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“…For tube formation analysis, human umbilical vein endothelial cells were seeded on Matrigel‐covered dishes as described and cultured with extracellular matrix (10% normal bovine serum albumin, and 1% penicillin/streptomycin and 1% endothelial cell growth supplement) containing concentrated fibroblast culture medium.…”

Section: Methodsmentioning

confidence: 99%

Haplodeficiency of Ataxia Telangiectasia Mutated Accelerates Heart Failure After Myocardial Infarction

Jia

Zhang

et al. 2017

JAHA

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BackgroundCell senescence is involved in the process of organ damage and repair; however, the underlying molecular mechanism needs to be further explored.Methods and ResultsSenescence‐related genes (ie, p21, p53, and ataxia telangiectasia mutated [ATM]) were shown to be elevated after myocardial infarction (MI) in both mouse and human hearts. Ten‐ to 12‐week‐old male wild‐type littermates (ATM +/+) and ATM heterozygous mice (ATM +/−) were subjected to MI. Cardiac echography showed that ATM haplodeficiency did not affect the survival rate but aggravated heart failure at day 28 post MI. Histologic analysis showed increased fibrosis in the noninfarct area of ATM +/− mice compared with that in ATM +/+ mice. Senescence‐associated β‐galactosidase staining showed that the number of senescent fibroblasts was decreased when ATM was haplodeficient both in vivo and in vitro. Costaining of α‐smooth muscle actin with p53 or p19 showed fewer senescent myofibroblasts in ATM +/− mouse hearts. Moreover, angiogenesis was also examined using the endothelial markers CD31 both at early (day 7) and late stages (day 28) after MI, and ATM haplodeficiency reduced angiogenesis after MI. Finally, cardiac fibroblasts were isolated from infarcted mouse heart and the medium were tested for its capacity of endothelial tubing formation, revealing that ATM haplodeficiency led to lower vascular endothelial growth factor production from cardiac fibroblast and reduced capacity of endothelial tube formation in vitro.ConclusionsThe present study shows that ATM haplodeficiency decreases fibroblast senescence and vascular endothelial growth factor production and impaired angiogenesis in response to MI, leading to accelerated heart failure.

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Deficiency of IL-12p35 improves cardiac repair after myocardial infarction by promoting angiogenesis

Abstract: Deficiency of IL-12p35 limited AMI-induced cardiac injury by promoting pro-angiogenesis and anti-inflammatory functions of monocytes.

Cited by 41 publications

References 47 publications

Roles and Mechanisms of Interleukin-12 Family Members in Cardiovascular Diseases: Opportunities and Challenges

Roles and Mechanisms of Interleukin-12 Family Members in Cardiovascular Diseases: Opportunities and Challenges

Inflammatory and non-inflammatory monocytes as novel prognostic biomarkers of survival in SOD1G93A mouse model of Amyotrophic Lateral Sclerosis

Haplodeficiency of Ataxia Telangiectasia Mutated Accelerates Heart Failure After Myocardial Infarction

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