The Role of Bone Morphogenetic Protein 7 (BMP-7) in Inflammation in Heart Diseases

Narasimhulu, Chandrakala Aluganti; Singla, Dinender K.

doi:10.3390/cells9020280

Cited by 62 publications

(45 citation statements)

References 251 publications

(317 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 10 , 27 , 48 This is highlighted by BMP7-driven attenuation of chondrocyte COX-2, IL-6, and PGE 2 levels in the present work, with similar actions for peptides p[63−82] and p[113−132]. BMP7 has previously also been reported as a morphogen with anti-inflammatory properties in other tissues and cell types like kidney, 49 heart, 50 blood vessels, 50 and macrophages. 51 The observation that these peptides attenuate PGE 2 release from intra-articular tissue other than cartilage (IPFP, meniscus, and not significantly from synovium) is in line with the previously reported tissue-wide anti-inflammatory actions of BMP7.…”

Section: Discussionsupporting

confidence: 78%

Discovery of bone morphogenetic protein 7-derived peptide sequences that attenuate the human osteoarthritic chondrocyte phenotype

Caron

Ripmeester

Akker

et al. 2021

Molecular Therapy - Methods & Clinical Development

View full text Add to dashboard Cite

Treatment of osteoarthritis (OA) is mainly symptomatic by alleviating pain to postpone total joint replacement. Bone morphogenetic protein 7 (BMP7) is a candidate morphogen for experimental OA treatment that favorably alters the chondrocyte and cartilage phenotype. Intra-articular delivery and sustained release of a recombinant growth factor for treating OA are challenging, whereas the use of peptide technology potentially circumvents many of these challenges. In this study, we screened a high-resolution BMP7 peptide library and discovered several overlapping peptide sequences from two regions in BMP7 with nanomolar bioactivity that attenuated the pathological OA chondrocyte phenotype. A single exposure of OA chondrocytes to peptides p[63−82] and p[113−132] ameliorated the OA chondrocyte phenotype for up to 8 days, and peptides were bioactive on chondrocytes in OA synovial fluid. Peptides p[63−82] and p[113−132] required NKX3-2 for their bioactivity on chondrocytes and provoke changes in SMAD signaling activity. The bioactivity of p[63−82] depended on specific evolutionary conserved sequence elements common to BMP family members. Intra-articular injection of a rat medial meniscal tear (MMT) model with peptide p[63−82] attenuated cartilage degeneration. Together, this study identified two regions in BMP7 from which bioactive peptides are able to attenuate the OA chondrocyte phenotype. These BMP7-derived peptides provide potential novel disease-modifying treatment options for OA.

show abstract

Section: Discussionsupporting

confidence: 78%

Discovery of bone morphogenetic protein 7-derived peptide sequences that attenuate the human osteoarthritic chondrocyte phenotype

Caron

Ripmeester

Akker

et al. 2021

Molecular Therapy - Methods & Clinical Development

View full text Add to dashboard Cite

show abstract

“…In addition, the KEGG pathway analysis of these differentially expressed genes showed that the top three signal pathways with the largest number of enriched genes were the TNF signaling pathway, osteoclast differentiation, and Toll-like receptor signaling pathway (Figure 2B). All these pathway enrichments were also supported and echoed by corresponding literature (13,27,28).…”

Section: Verification and Functional Analysis Of Differentially Expressed Genes In Acute MIsupporting

confidence: 85%

Development and Validation of a Random Forest Diagnostic Model of Acute Myocardial Infarction Based on Ferroptosis-Related Genes in Circulating Endothelial Cells

Chen

Shi

2021

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

The high incidence and mortality of acute myocardial infarction (MI) drastically threaten human life and health. In the past few decades, the rise of reperfusion therapy has significantly reduced the mortality rate, but the MI diagnosis is still by means of the identification of myocardial injury markers without highly specific biomarkers of microcirculation disorders. Ferroptosis is a novel reported type of programmed cell death, which plays an important role in cancer development. Maintaining iron homeostasis in cells is essential for heart function, and its role in the pathological process of ischemic organ damages remains unclear. Being quickly detected through blood tests, circulating endothelial cells (CECs) have the potential for early judgment of early microcirculation disorders. In order to explore the role of ferroptosis-related genes in the early diagnosis of acute MI, we relied on two data sets from the GEO database to first detect eight ferroptosis-related genes differentially expressed in CECs between the MI and healthy groups in this study. After comparing different supervised learning algorithms, we constructed a random forest diagnosis model for acute MI based on these ferroptosis-related genes with a compelling diagnostic performance in both the validation (AUC = 0.8550) and test set (AUC = 0.7308), respectively. These results suggest that the ferroptosis-related genes might play an important role in the early stage of MI and have the potential as specific diagnostic biomarkers for MI.

show abstract

“…Five viral miRNAs were predicted to act in synergy to regulate 2 genes (BMP7 and CD36) out of 4 significantly down-regulated genes related to immune and apoptotic functions. Previous studies reported that BMP-7 is associated with pathophysiology of several diseases[ 48 ]. Recent evidence suggested that antagonists of BMP signaling pathways may play critical role in the treatment of COVID-19 induced multi-organ failure[ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Decrypting the role of predicted SARS-CoV-2 miRNAs in COVID-19 pathogenesis: A bioinformatics approach

Rahaman

Komanapalli

Mukherjee

et al. 2021

Computers in Biology and Medicine

View full text Add to dashboard Cite

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is a highly transmissible virus causing the ongoing global pandemic, COVID-19. Evidence suggests that viral and host microRNAs play pivotal roles in progression of such infections. The decisive impact of viral miRNAs and their putative targets in modulating the transcriptomic profile of its host, however remains unexplored. We hypothesized that the SARS-CoV-2 derived miRNAs can potentially play a contributory role in its pathogenicity and aid in its survival. A series of computational tools predicted 34 SARS-CoV-2 encoded miRNAs and their putative targets in the host. Immune and apoptotic pathways were identified as most enriched pathways. Further investigation using a dataset of SARS-CoV-2 infected cells (available from public repository- GSE150392) revealed that 46 genes related to immune and apoptosis-related functions were deregulated. Of these 46 genes, 42 genes were identified to be significantly up-regulated and 4 genes were down-regulated . In silico analysis revealed all of the these significantly down-regulated genes to be putative targets of 9 out of 34 of our predicted viral miRNAs. Overall, 123 out of 324 genes that are differentially regulated in SARS-CoV2 infected cells, and also identified as putative targets of viral miRNAs, were found to be significantly down-regulated. KEGG pathway analysis using these genes revealed p53 signaling as the most enriched pathway – a pathway that is known to influence immune responses. This study thus provides the theoretical foundation for the underlying molecular mechanisms involved in progression of viral pathogenesis.

show abstract

The Role of Bone Morphogenetic Protein 7 (BMP-7) in Inflammation in Heart Diseases

Cited by 62 publications

References 251 publications

Discovery of bone morphogenetic protein 7-derived peptide sequences that attenuate the human osteoarthritic chondrocyte phenotype

Discovery of bone morphogenetic protein 7-derived peptide sequences that attenuate the human osteoarthritic chondrocyte phenotype

Development and Validation of a Random Forest Diagnostic Model of Acute Myocardial Infarction Based on Ferroptosis-Related Genes in Circulating Endothelial Cells

Decrypting the role of predicted SARS-CoV-2 miRNAs in COVID-19 pathogenesis: A bioinformatics approach

Contact Info

Product

Resources

About