Possible involvement of SDF-1/CXCL12 in the pathogenesis of Degos disease

Meephansan, Jitlada; Komine, Mayumi; Hosoda, Satomi; Tsuda, Hidetoshi; Karakawa, Masaru; Murata, Satoru; Demitsu, Toshio; Ohtsuki, Mamitaro

doi:10.1016/j.jaad.2012.06.031

Cited by 15 publications

(29 citation statements)

References 29 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistently, miR‐103a‐3p was downregulated in plasmas of venous thromboembolism (VTE) patients as compared with controls . SDF‐1/CXCL12 has been noted to induce thrombosis . Previous evidence has suggested that venous thrombus resolution, an inflammatory process, is dependent on chemokines .…”

Section: Discussionmentioning

confidence: 82%

See 1 more Smart Citation

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

et al. 2019

View full text Add to dashboard Cite

Studies have shown that microRNAs (miRNAs) participate in almost all pathological and physiological processes including acute lower‐extremity deep venous thrombosis (LEDVT). Here, this study was designed to elucidate the possible function of miR‐103a‐3p in acute LEDVT. Expression of miR‐103a‐3p and chemokine C‐X‐C motif ligand 12 (CXCL12) was initially quantified in plasma collected from 81 LEDVT patients. Then LEDVT mouse models were established by injection with 3% sodium pentobarbital. The interaction between miR‐103a‐3p and CXCL12 was identified by dual‐luciferase reporter gene assay. After gain‐ and loss‐of‐function studies, interleukin‐6 (IL‐6) and IL‐8 and tissue factor (TF) levels, and expression of plasminogen activator inhibitors (PAIs), von Willebrand factor (vWF), thromboxane A2 (TH‐A2), F4/80, IL‐12, Arginase‐1 (Arg‐1) and CD206 were determined using enzyme‐linked immunosorbent assay (ELISA), reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis, respectively. miR‐103a‐3p was downregulated, while CXCL12 was upregulated in patients and mice with LEDVT. miR‐103a‐3p targets CXCL12 and inhibited its expression. Overexpressed miR‐103a‐3p or downregulated CXCL12 decreased expression of IL‐6, IL‐8, TF, PAIs, vWF, TH‐A2, M1 markers (IL‐6 and IL‐12), yet increased expression of M2 markers (Arg‐1 and CD206) in LEDVT mice. Additionally, upregulated miR‐103a‐3p or silencing CXCL12 suppressed thrombosis in LEDVT mice. However, overexpression of CXCL12 reversed the tendency mentioned above. Altogether, miR‐103a‐3p can potentially downregulate CXCL12 expression to disrupt inflammatory response and thrombosis, ultimately preventing the development of LEDVT. Our findings underscore a possible alternative therapeutic strategy to limit LEDVT.

show abstract

Section: Discussionmentioning

confidence: 82%

“…23 SDF-1/CXCL12 has been noted to induce thrombosis. 24 Previous evidence has suggested that venous thrombus resolution, an inflammatory process, is dependent on chemokines. 25 In addition, CXCL12 has been found to emerge as a crucial therapeutic target for thrombosis.…”

Section: Mir-103a-3p Regulates Macrophage Polarization and Venous Tmentioning

confidence: 99%

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

et al. 2019

View full text Add to dashboard Cite

show abstract

“…All these observations may provide an explanation for the pathogenesis of MAP. Currently, Meephansan et al [41] observed strong staining of the infiltrating inflammatory cells in the perivascular, intravascular, and perineural areas in tissue samples from 2 MAP patients with stromal cell–derived factor (SDF)-1/CXCL12, which is secreted by bone-marrow stromal and endothelial cells, activates megakaryocyte precursors, and costimulates platelet activation.…”

Section: Introductionmentioning

confidence: 99%

Malignant atrophic papulosis (Köhlmeier-Degos disease) - A review

Theodoridis

Makrantonaki

Zouboulis

2013

Orphanet J Rare Dis

172

View full text Add to dashboard Cite

Definition of the diseaseMalignant atrophic papulosis (MAP), described independently by Köhlmeier and Degos et al., is a rare, chronic, thrombo-obliterative vasculopathy characterized by papular skin lesions with central porcelain-white atrophy and surrounding teleangiectatic rim.EpidemiologyLess than 200 cases have been described in the literature. The first manifestation of MAP usually occurs between the 20th and 50th year of life.Clinical descriptionThe cutaneous clinical picture is almost pathognomonic. The histology is not consistent but in most cases it shows a wedge-shaped connective tissue necrosis in the deep corium due to a thrombotic occlusion of the small arteries. In the systemic variant, manifestations mostly occur at the intestine and central nervous system.EtiologyThe etiopathogenesis of the disease remains unknown, a genetic predisposition may occur. Vasculitis, coagulopathy or primary dysfunction of the endothelial cells have been implicated.Diagnostic methodsDiagnosis is only based on the characteristic skin lesions.Differrential diagnosisIt depends on the clinical presentation of MAP, but systemic lupus erythematosus and other connective tissue diseases need to be considered.ManagementNo effective treatment exists for the systemic manifestations, while compounds that facilitate blood perfusion have achieved a partial regression of the skin lesions in single cases.PrognosisAn apparently idiopathic, monosymptomatic, cutaneous, benign variant and a progressive, visceral one with approx. 50% lethality within 2–3 years have been reported. Systemic manifestations can develop years after the occurrence of skin lesions leading to bowel perforation and peritonitis, thrombosis of the cerebral arteries or massive intracerebral hemorrhage, meningitis, encephalitis, radiculopathy, myelitis.

show abstract

“…In a recent study carried out on patients with atrophic papulosis, a strong lymphocyte expression of a stromal cell‐derived factor‐1, a chemokine that activates platelets, has been shown. Thus, this chemokine seems to play a role in the pathogenesis of atrophic papulosis …”

mentioning

confidence: 99%

Benign form of atrophic papulosis developed at injection sites of pegylated-alpha-interferon: is there a pathophysiological link?

et al. 2014

View full text Add to dashboard Cite

by Ramos et al., 10 a large number of genetic, epigenetic, regulatory and environmental factors are involved in the development of SLE. Thus PTEN deficiency may be just one of many contributory factors in a subset of cases. However, the current evidence does seem to support the idea that decreased expression of PTEN, by mutations or by miRNA, may play a role in SLE pathogenesis. Further investigations into the cause of increased miR-17-92 cluster expression in patients with SLE, as well as characterization of the frequency of positive serum lupus markers in patients with PHTS, are warranted.

show abstract

Possible involvement of SDF-1/CXCL12 in the pathogenesis of Degos disease

Cited by 15 publications

References 29 publications

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

Malignant atrophic papulosis (Köhlmeier-Degos disease) - A review

Benign form of atrophic papulosis developed at injection sites of pegylated-alpha-interferon: is there a pathophysiological link?

Contact Info

Product

Resources

About