904 nm Low-Level Laser Irradiation Decreases Expression of Catabolism-Related Genes in White Adipose Tissue of Wistar Rats: Possible Roles of Laser on Metabolism.

Background: Adipose tissue is the main energy storage tissue in the body. Its catabolic and anabolic responses depend on several factors, such as nutritional status, metabolic profile, and hormonal signaling. There are few studies addressing the effects of laser photobiomodulation (PBM) on adipose tissue and results are controversial. Objective: Our purpose was to investigate the metabolic effects of PBM on adipose tissue from Wistar rats supplemented or not with caffeine. Materials and methods: Wistar rats were divided into four groups: control (CTL), laser-treated [CTL (L)], caffeine (CAF), and caffeine+PBM [CAF (L)]. Blood was extracted for quantification of triglyceride and cholesterol levels and white adipose tissues were collected for analysis. We evaluated gene expression in the adipose tissue for the leptin receptor, lipase-sensitive hormone, tumor necrosis factor alpha, and beta adrenergic receptor. Results: We demonstrated that the low-level laser irradiation was able to increase the feed intake of the animals and the relative mass of the adipose tissue in the CTL (L) group compared with CTL. Laser treatment also increases serum triglycerides [CTL = 46.99 ± 5.87; CTL (L) = 57.46 ± 14.38; CAF = 43.98 ± 5.17; and CAF (L) = 56.9 ± 6.12; p = 0.007] and total cholesterol (CTL = 70.62 ± 6.80; CTL (L) = 79.41 ± 13.07; CAF = 71.01 ± 5.52; and CAF (L) = 79.23 ± 6.881; p = 0.003). Conclusions: Laser PBM decreased gene expression of the studied genes in the adipose tissue, indicating that PBM is able to block the catabolic responses of this tissue. Interestingly, the CAF (L) and CAF animals presented the same CLT (L) phenotype, however, without increasing the feed intake and the relative weight of the adipose tissue. The description of these phenomena opens a new perspective for the study of the action of low-level laser in adipose tissue.

Treatment with Mesenchymal Stem Cells Improves Renovascular Hypertension and Preserves the Ability of the Contralateral Kidney to Excrete Sodium.

BACKGROUND: Mesenchymal stem cells (MSC) improve renal function and renovascular hypertension in the 2-kidney 1-clip model (2K-1C). While MSC play an immunomodulatory role, induce neoangiogenesis, and reduce fibrosis, they do not correct sodium loss by the contra-lateral kidney. OBJECTIVES: We investigated the tubular function of both stenotic and contralateral kidneys and the effect of MSC treatment by evaluating diuresis, natriuresis, and the expression of the main water and sodium transporters. METHOD: Adult Wistar rats were allocated into four groups: control (CT), CT+MSC, 2K-1C, and 2K-1C+MSC. MSC (2 × 105) were infused through the tail vein 3 and 5 weeks after clipping. Systolic blood pressure (SBP) was monitored weekly by plethysmography. Six weeks after clipping, 24-hour urine and blood samples were collected for biochemical analysis. Gene expression of the Na/H exchanger-3, epithelial sodium channel, Na/K-ATPase, Na/K/2Cl cotransporter, and aquaporins 1 and 2 (AQP1 and AQP2) were analyzed by RT-PCR. Intrarenal distribution of AQP1 and AQP2 was analyzed by immunohistochemistry. RESULTS: In hypertensive 2K-1C animals, MSC prevented additional increases in BP. AQP1, but not AQP2, was suppressed in the contralateral kidney, resulting in significant increase in urinary flow rate and sodium excretion. Gene expressions of sodium transporters were similar in both kidneys, suggesting that the high perfusing pressure in the contralateral kidney was responsible for increased natriuresis. Contralateral hypertensive kidney showed signs of renal deterioration with lower GFR in spite of normal RPF levels. CONCLUSIONS: MSC treatment improved renal function and enhanced the ability of the contralateral kidney to excrete sodium through a tubular independent mechanism contributing to reduce SBP.

Laser Photobiomodulation 904 nm Promotes Inhibition of Hormone-Sensitive Lipase Activity in 3T3-L1 Adipocytes Differentiated Cells.

Background: The lipid metabolism is essential for maintaining the body's energy responses. Laser photobiomodulation triggers many important cellular effects, but these effects on lipid metabolism are not well described. In this study, we analyzed the laser photobiomodulation in the hormone-sensitive lipase (HSL) activity, a key enzyme in the triglycerides (TAG) hydrolysis in adipose tissue 3T3-L1. Methods: Cells were submitted to the differentiation protocol in adipose cells, irradiated with 1, 2, and 3J with laser (904 nm-60 mw-laser diode) and incubated for 4 h after irradiation. Results: The response of laser photobiomodulation was able to trigger an inhibition of HSL activity (control = 0.057 ± 0.0008; 1J = 0.050 ± 0.0003; 2J = 0.0477 ± 0.002; 3J = 0.051 ± 0.002; p = 0.0003 against the control), but no modulation was observed in TAG levels into the medium (control = 26.5856 ± 0.52; 1J = 26.5856 ± 0.52; 2J = 27.2372 ± 1.41; 3J = 25.9991 ± 0.1303; p = 0.18). Conclusions: This is the first study of HSL activity modulation with laser radiation, suggesting that photobiomodulation can influence adipose tissue metabolism and open a new field of study.

The angiotensin-I-converting enzyme insertion/deletion in polymorphic element codes for an AluYa5 RNA that downregulates gene expression.

Angiotensin-I-converting enzyme (ACE) is involved in the synthesis and degradation of important bioactive peptides. The ACE gene has a 287-bp insertion/deletion polymorphism that controls ACE expression through a mechanism that remains elusive. In this study, we found that the 287-bp polymorphic element of the ACE gene, a member of the AluYa5 sub-family of Alu elements, codes for an RNA molecule that controls the levels of ACE mRNA. Transient transfection of a plasmid containing a CMV promoter upstream of the ACE polymorphic element resulted in significant expression of an AluYa5 RNA and reduced ACE mRNA expression as well as ACE enzymatic activity in AD 293 cells. The AluYa5 element also independently reduced the expression of other genes, regardless of whether these genes harbored Alu elements within their genomic context. Interestingly, the CMV promoter was not required for the expression of the AluYa5 element in AD 293 cells. The 287-bp sequence was sufficient to produce AluYa5 RNA and led to a significant reduction in ACE gene expression. Moreover, the removal of an 11-bp fragment of the 3' end of the ACE polymorphic sequence, which is specific to this particular AluYa5 element, did not prevent this element from being expressed but did affect its ability to target ACE expression. Thus, the expression of the AluYa5 polymorphic element within the ACE gene could explain why patients carrying the ACE insertion polymorphism have reduced risk of developing several chronic diseases.