High ApoD protein level in the round ligament fat depot of severely obese women is associated with an improved inflammatory profile

Desmarais, Frédérik; Bergeron, Karl-F.; Lacaille, Michel; Lemieux, Isabelle; Bergeron, Jean; Biron, Simon; Rassart, Éric; Joanisse, Denis R.; Mauriège, Pascale; Mounier, Cathérine

doi:10.1007/s12020-018-1621-5

Cited by 22 publications

(21 citation statements)

References 54 publications

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“…Specifically, protein levels of ApoD in the human MAT were associated with reduced circulating TNF-α and improved insulin sensitivity (QUICKY index). These correlations did not exist with ApoD mRNA expression [64] suggesting that circulating ApoD, after adipose tissue internalization, was specifically responsible for this association. This hypothesis is reinforced by our present results, which indicate that circulating hApoD can accumulate in the MAT.…”

Section: Discussionmentioning

confidence: 79%

Cerebral Apolipoprotein D Exits the Brain and Accumulates in Peripheral Tissues

Desmarais

Hervé

Bergeron

et al. 2021

IJMS

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Apolipoprotein D (ApoD) is a secreted lipocalin associated with neuroprotection and lipid metabolism. In rodent, the bulk of its expression occurs in the central nervous system. Despite this, ApoD has profound effects in peripheral tissues, indicating that neural ApoD may reach peripheral organs. We endeavor to determine if cerebral ApoD can reach the circulation and accumulate in peripheral tissues. Three hours was necessary for over 40% of all the radiolabeled human ApoD (hApoD), injected bilaterally, to exit the central nervous system (CNS). Once in circulation, hApoD accumulates mostly in the kidneys/urine, liver, and muscles. Accumulation specificity of hApoD in these tissues was strongly correlated with the expression of lowly glycosylated basigin (BSG, CD147). hApoD was observed to pass through bEnd.3 blood brain barrier endothelial cells monolayers. However, cyclophilin A did not impact hApoD internalization rates in bEnd.3, indicating that ApoD exit from the brain is either independent of BSG or relies on additional cell types. Overall, our data showed that ApoD can quickly and efficiently exit the CNS and reach the liver and kidneys/urine, organs linked to the recycling and excretion of lipids and toxins. This indicated that cerebral overexpression during neurodegenerative episodes may serve to evacuate neurotoxic ApoD ligands from the CNS.

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Section: Discussionmentioning

confidence: 79%

Cerebral Apolipoprotein D Exits the Brain and Accumulates in Peripheral Tissues

Desmarais

Hervé

Bergeron

et al. 2021

IJMS

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“…Tsukamoto et al reported altered response to myocardial infarction in Apod knockout mice [37], revealing APOD as a cardioprotective gene using a mouse model of lethal atherosclerotic coronary artery disease. In addition, high levels of APOD protein in humans are associated with protective inflammatory levels and fatty liver in initial human studies [38,39]. Further investigation of APOD in mouse models and larger human studies will be needed for experimental validation of this mechanism, and to allow investigation of underlying mechanisms related to atherosclerotic coronary artery disease.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide transcriptome study using deep RNA sequencing for myocardial infarction and coronary artery calcification

et al. 2021

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Background Coronary artery calcification (CAC) is a noninvasive measure of coronary atherosclerosis, the proximal pathophysiology underlying most cases of myocardial infarction (MI). We sought to identify expression signatures of early MI and subclinical atherosclerosis in the Framingham Heart Study (FHS). In this study, we conducted paired-end RNA sequencing on whole blood collected from 198 FHS participants (55 with a history of early MI, 72 with high CAC without prior MI, and 71 controls free of elevated CAC levels or history of MI). We applied DESeq2 to identify coding-genes and long intergenic noncoding RNAs (lincRNAs) differentially expressed in MI and high CAC, respectively, compared with the control. Results On average, 150 million paired-end reads were obtained for each sample. At the false discovery rate (FDR) < 0.1, we found 68 coding genes and 2 lincRNAs that were differentially expressed in early MI versus controls. Among them, 60 coding genes were detectable and thus tested in an independent RNA-Seq data of 807 individuals from the Rotterdam Study, and 8 genes were supported by p value and direction of the effect. Immune response, lipid metabolic process, and interferon regulatory factor were enriched in these 68 genes. By contrast, only 3 coding genes and 1 lincRNA were differentially expressed in high CAC versus controls. APOD, encoding a component of high-density lipoprotein, was significantly downregulated in both early MI (FDR = 0.007) and high CAC (FDR = 0.01) compared with controls. Conclusions We identified transcriptomic signatures of early MI that include differentially expressed protein-coding genes and lincRNAs, suggesting important roles for protein-coding genes and lincRNAs in the pathogenesis of MI.

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“…Although Th17 cells were initially investigated in RA due to their potency against autoimmune diseases [ 59 ], accumulating evidence suggests they are also increased in the OA [ 60 ]. Additionally, the high APOD protein level in the round ligament fat depot of severely obese women is associated with an improved inflammatory profile [ 61 ]. Thus, APOD may manage OA through chondrogenesis in articular cartilage and immune regulation in the synovium.…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Targets of Knee Osteoarthritis Shared by Cartilage and Synovial Tissue

Zheng

2020

IJMS

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Arthritis is the leading cause of disability among adults, while osteoarthritis (OA) is the most common form of arthritis that results in cartilage loss. However, accumulating evidence suggests that the protective hyaline cartilage should not be the sole focus of OA treatment. Particularly, synovium also plays essential roles in OA’s initiation and progression and warrants serious consideration when battling against OA. Thus, biomarkers with similar OA-responsive expressions in cartilage and synovium should be the potential targets for OA treatment. On the other hand, molecules with a distinguished response during OA in cartilage and synovium should be ruled out as OA therapeutic(s) to avoid controversial effects in different tissues. Here, to pave the path for developing a new generation of OA therapeutics, two published transcriptome datasets of knee articular cartilage and synovium were analyzed in-depth. Genes with statistically significantly different expression in OA and healthy cartilage were compared with those in the synovium. Thirty-five genes with similar OA-responsive expression in both tissues were identified while recognizing three genes with opposite OA-responsive alteration trends in cartilage and synovium. These genes were clustered based on the currently available knowledge, and the potential impacts of these clusters in OA were explored.

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High ApoD protein level in the round ligament fat depot of severely obese women is associated with an improved inflammatory profile

Cited by 22 publications

References 54 publications

Cerebral Apolipoprotein D Exits the Brain and Accumulates in Peripheral Tissues

Cerebral Apolipoprotein D Exits the Brain and Accumulates in Peripheral Tissues

Genome-wide transcriptome study using deep RNA sequencing for myocardial infarction and coronary artery calcification

Identification of Novel Targets of Knee Osteoarthritis Shared by Cartilage and Synovial Tissue

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