Vitamin D status influences cytokine production and MALAT1 expression from the PBMCs of patients with coronary artery disease and healthy controls.

OBJECTIVE: This study aimed to investigate the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) expression and its role in cytokine production from peripheral blood mononuclear cells (PBMCs) in patients with coronary artery disease (CAD) and non-CAD participants (NCAD). METHODS: Blood samples were taken from 15 patients with CAD and 15 NCAD individuals. The plasma was used for biochemical analyses. MALAT1 and CD36 expressions were evaluated in the isolated peripheral blood mononuclear cells (PBMCs) by real-time PCR. Furthermore, the levels of inflammatory cytokines e.g. interleukin (IL)-6, IL-10, and IL-22 were measured in the supernatants of the cultured PBMCs by flow cytometry. RESULTS: The levels of MALAT1 and CD36 were not significantly different between the CAD and NCAD groups. However, a lower level of MALAT1 and CD36 was observed in PBMCs of vitamin D deficient (<15 ng/ml) CAD and NCAD participants. Furthermore, the vitamin D deficient (<15 ng/ml) group showed a significantly higher plasma level of IL-6, IL-10, and IL-22 compared to the non-deficient (≥15 ng/ml) group. In addition, significant positive correlations were found between CD36, IL-22, and fasting blood sugar (FBS) with MALAT1. CONCLUSION: Given that in vitamin D deficient individuals a decreased level of MALAT1 was associated with CD36 expression and increased IL-22 production, vitamin D supplementation may play a role in reducing MALAT1/CD36/IL-22 mediated complications such as T2DM and CAD, especially in vitamin D deficiency.

Vitamin D status influences cytokine production and MALAT1 expression from the PBMCs of patients with coronary artery disease and healthy controls

SUMMARY OBJECTIVE: This study aimed to investigate the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) expression and its role in cytokine production from peripheral blood mononuclear cells (PBMCs) in patients with coronary artery disease (CAD) and non-CAD participants (NCAD). METHODS: Blood samples were taken from 15 patients with CAD and 15 NCAD individuals. The plasma was used for biochemical analyses. MALAT1 and CD36 expressions were evaluated in the isolated peripheral blood mononuclear cells (PBMCs) by real-time PCR. Furthermore, the levels of inflammatory cytokines e.g. interleukin (IL)-6, IL-10, and IL-22 were measured in the supernatants of the cultured PBMCs by flow cytometry. RESULTS: The levels of MALAT1 and CD36 were not significantly different between the CAD and NCAD groups. However, a lower level of MALAT1 and CD36 was observed in PBMCs of vitamin D deficient (<15 ng/ml) CAD and NCAD participants. Furthermore, the vitamin D deficient (<15 ng/ml) group showed a significantly higher plasma level of IL-6, IL-10, and IL-22 compared to the non-deficient (≥15 ng/ml) group. In addition, significant positive correlations were found between CD36, IL-22, and fasting blood sugar (FBS) with MALAT1. CONCLUSION: Given that in vitamin D deficient individuals a decreased level of MALAT1 was associated with CD36 expression and increased IL-22 production, vitamin D supplementation may play a role in reducing MALAT1/CD36/IL-22 mediated complications such as T2DM and CAD, especially in vitamin D deficiency.

RESUMO OBJETIVO: O objetivo deste estudo foi investigar a expressão do RNA longo não codificante lncRNA MALAT1 e o seu papel na produção de citocinas a partir de células mononucleares do sangue periférico (PBMCs) em pacientes com doença arterial coronariana (DAC) e participantes sem DAC (NDAC). MÉTODOS: Amostras de sangue foram coletadas de 15 pacientes com DAC e 15 indivíduos NCAD. O plasma foi usado para análises bioquímicas. As expressões de MALAT1 e CD36 foram avaliadas nas células mononucleares do sangue periférico (PBMCs) isoladas por PCR em tempo real. Além disso, os níveis de citocinas inflamatórias, como a interleucina (IL)-6, IL-10 e IL-22 foram medidas no sobrenadante da cultura de PBMCs por citometria de fluxo. RESULTADOS: Os níveis de MALAT1 e CD36 não foram significativamente diferentes entre os grupos DAC e NDAC. No entanto, um nível inferior de MALAT1 e CD36 foi observado nas PBMCs de participantes com deficiência de vitamina D (< 15 ng/ml) tanto no grupo DAC quanto no NDAC. Além disso, o grupo com deficiência de vitamina D (< 15 ng/ml) apresentou um nível plasmático significativamente maior de IL-6, IL-10 e IL-22 em comparação com o grupo sem a deficiência (≥15 ng/ml). Além disso, foram encontradas correlações positivas significativas entre CD36, IL-22, e glicemia de jejum (GJ) e o MALAT1. CONCLUSÃO: Dado que em indivíduos com deficiência de vitamina D a diminuição do nível de MALAT1 foi associada com a expressão de CD36 e produção aumentada de IL-22, a suplementação de vitamina D pode ter um papel importante na redução de complicações mediadas por MALAT1/CD36/IL-22, tais como DMT2 e DAC, especialmente em casos de deficiência de vitamina D.