LRP1: A chameleon receptor of lung inflammation and repair

Wujak, Lukasz; Schnieder, Jennifer; Schaefer, Liliana; Wygrecka, Małgorzata

doi:10.1016/j.matbio.2017.12.007

Cited by 33 publications

(31 citation statements)

References 126 publications

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“…[30][31][32] Thus, inhibition of p38/JNK and NF-κB pathways has been considered as effective strategy for treating COPD. 40 33,34 The results indicated that gastrodin prevented LPS-induced injury in MRC-5 cells through these two signalling.…”

Section: Lps-induced Inflammatory Injury Besides That Gastrodin Is mentioning

confidence: 83%

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Qiao

Wang

et al. 2019

J Cellular Molecular Medi

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The beneficial function of gastrodin towards many inflammatory diseases has been identified. This study designed to see the influence of gastrodin in a cell model of chronic obstructive pulmonary disease (COPD). MRC‐5 cells were treated by LPS, before which gastrodin was administrated. The effects of gastrodin were evaluated by conducting CCK‐8, FITC‐PI double staining, Western blot, qRT‐PCR and ELISA. Besides this, the downstream effector and signalling were studied to decode how gastrodin exerted its function. And dual‐luciferase assay was used to detect the targeting link between miR‐103 and lipoprotein receptor‐related protein 1 (LRP1). LPS induced apoptosis and the release of MCP‐1, IL‐6 and TNF‐α in MRC‐5 cells. Pre‐treating MRC‐5 cells with gastrodin attenuated LPS‐induced cell damage. Meanwhile, p38/JNK and NF‐κB pathways induced by LPS were repressed by gastrodin. miR‐103 expression was elevated by gastrodin. Further, the protective functions of gastrodin were attenuated by miR‐103 silencing. And LRP1 was a target of miR‐103 and negatively regulated by miR‐103. The in vitro data illustrated the protective function of gastrodin in LPS‐injured MRC‐5 cells. Gastrodin exerted its function possibly by up‐regulating miR‐103 and modulating p38/JNK and NF‐κB pathways.

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Section: Lps-induced Inflammatory Injury Besides That Gastrodin Is mentioning

confidence: 83%

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Qiao

Wang

et al. 2019

J Cellular Molecular Medi

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“…Cellular responses appear to be cell type specific and possibly vary depending on which ligand engages LRP1: For example, tissue plasminogen activator binding to LRP1 engages signaling through integrins that has profibrotic effects on kidney interstitial fibroblasts. [119][120][121][122][123] Ultimately, direct examination of TSP1 N-terminal domain binding to calreticulin-LRP1 on collagen organization in fibrotic remodeling remains to be addressed using TSP-binding calreticulin peptides that block TSP1-calreticulin interactions in animal models. 13,99 The TSP family has been long known to play a role in the regulation of collagenous ECM fibril organization.…”

Section: Tsp1 As a Regulator Of Collagen Matrix Organizationmentioning

confidence: 99%

Thrombospondin 1 and Its Diverse Roles as a Regulator of Extracellular Matrix in Fibrotic Disease

Murphy-Ullrich

2019

J Histochem Cytochem.

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Thrombospondin 1 (TSP1) is a matricellular extracellular matrix protein that has diverse roles in regulating cellular processes important for the pathogenesis of fibrotic diseases. We will present evidence for the importance of TSP1 control of latent transforming growth factor beta activation in renal fibrosis with an emphasis on diabetic nephropathy. Other functions of TSP1 that affect renal fibrosis, including regulation of inflammation and capillary density, will be addressed. Emerging roles for TSP1 N-terminal domain regulation of collagen matrix assembly, direct effects of TSP1-collagen binding, and intracellular functions of TSP1 in mediating endoplasmic reticulum stress responses in extracellular matrix remodeling and fibrosis, which could potentially affect renal fibrogenesis, will also be discussed. Finally, we will address possible strategies for targeting TSP1 functions to treat fibrotic renal disease. (J Histochem Cytochem 67: 683-699, 2019)

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“…Identification of novel pro- and anti-inflammatory factors and pathways remains an important challenge for addressing these disease states. Recent research has shown that LRP1 modulates several of these inflammatory pathways (30, 41) (Figure 4).…”

Section: Low-density Lipoprotein Receptor-related Protein 1 (Lrp1): Gmentioning

confidence: 99%

“…Upon LPS recognition, TLR4 activates a complex intracellular signaling network ultimately resulting in the translocation of the transcription factors interferon regulatory factor 3 (IRF-3) and NF-κB to the nucleus, and the expression of pro-inflammatory genes (42). Various studies revealed that LRP1 limits the LPS-induced inflammatory response in multiple cell types and experimental models of injury (30, 41).…”

Section: Low-density Lipoprotein Receptor-related Protein 1 (Lrp1): Gmentioning

confidence: 99%

Low Density Lipoprotein Receptor-Related Protein-1 in Cardiac Inflammation and Infarct Healing

Potere

Buono

Mauro

et al. 2019

Front. Cardiovasc. Med.

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Acute myocardial infarction (AMI) leads to myocardial cell death and ensuing sterile inflammatory response, which represents an attempt to clear cellular debris and promote cardiac repair. However, an overwhelming, unopposed or unresolved inflammatory response following AMI leads to further injury, worse remodeling and heart failure (HF). Additional therapies are therefore warranted to blunt the inflammatory response associated with ischemia and reperfusion and prevent long-term adverse events. Low-density lipoprotein receptor-related protein 1 (LRP1) is a ubiquitous endocytic cell surface receptor with the ability to recognize a wide range of structurally and functionally diverse ligands. LRP1 transduces multiple intracellular signal pathways regulating the inflammatory reaction, tissue remodeling and cell survival after organ injury. In preclinical studies, activation of LRP1-mediated signaling in the heart with non-selective and selective LRP1 agonists is linked with a powerful cardioprotective effect, reducing infarct size and cardiac dysfunction after AMI. The data from early phase clinical studies with plasma-derived α1-antitrypsin (AAT), an endogenous LRP1 agonist, and SP16 peptide, a synthetic LRP1 agonist, support the translational value of LRP1 as a novel therapeutic target in AMI. In this review, we will summarize the cellular and molecular bases of LRP1 functions in modulating the inflammatory reaction and the reparative process after injury in various peripheral tissues, and discuss recent evidences implicating LRP1 in myocardial inflammation and infarct healing.

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LRP1: A chameleon receptor of lung inflammation and repair

Cited by 33 publications

References 126 publications

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Thrombospondin 1 and Its Diverse Roles as a Regulator of Extracellular Matrix in Fibrotic Disease

Low Density Lipoprotein Receptor-Related Protein-1 in Cardiac Inflammation and Infarct Healing

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