Energy-dependent effect trial of photobiomodulation on blood pressure in hypertensive rats.

The main purpose of this work was to construct an energy-dependent response curve of photobiomodulation on arterial pressure in hypertension animal model. To reach this objective, we have used a two-kidney one clip (2K-1C) rat model. Animals received acute laser light irradiation (660 nm) on abdominal region using different energy (0.6, 1.8, 3.6, 7.2, 13.8, 28.2, 55.8, and 111.6 J), the direct arterial pressure was measured by femoral cannulation, and systolic arterial pressure (SAP), diastolic arterial pressure (DAP), heart rate (HR), and time of effect were obtained. Our results indicated that 660 nm laser light presents an energy-dependent hypotensive effect, and 28.2 J energy irradiation reached the maximum hypotensive effect, inducing a decreased SAP, DAP, and HR (decrease in SAP: - 19.23 ± 1.82 mmHg, n = 11; DAP: - 9.57 ± 2.23 mmHg, n = 11; HR: - 39.15 ± 5.10 bpm, n = 11; and time of hypotensive effect: 3068.00 ± 719.00 s, n = 11). The higher energy irradiation evaluated (111.6 J) did not induce a hypotensive effect and induced an increase in HR (21.69 ± 7.89 bpm, n = 7). Taken together, our results indicate that red laser energy irradiation from 7.2 to 55.8 J is the effective therapeutic window to reduce SAP, DAP, MAP, and HR and induce a long-lasting hypotensive effect in rats, with effect loss at higher energy irradiation (111.6 J).

Hypotensive acute effect of photobiomodulation therapy on hypertensive rats.

The purpose of this study was to evaluate the acute effect of photobiomodulation therapy (PBM) on arterial pressure in hypertensive and normotensive rats with application in an abdominal region. Normotensive (2K) and hypertensive (2K-1C) wistar rats were treated with PBM. Systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP) and heart rate (HR) were measured before, during and after PBM application. The nitric oxide (NO) serum concentration was measured before and after PBM application. Vascular reactivity study was performed in isolated thoracic aortas. Aluminum gallium arsenide (GaAlAs) diode laser was used, at 660nm wavelength and 100mW optical output. The PBM application induced a decrease of SAP in 2K-1C rats. In 2K rats, the PBM application had no effect on SAP, DAP and MAP. Moreover, the magnitude of hypotensive effect was higher in 2K-1C than in 2K rats. The PBM application induced a decrease of HR in 2K-1C and 2K, with higher effect in 2K-1C rats. In 2K-1C, the hypotensive effect induced by PBM was longer than that obtained in 2K rats. PBM application induced an elevation of NO concentration in serum from 2K-1C and 2K rats, with higher effect in 2K-1C. In isolated aortic rings PBM effect is dependent of NO release, and is not dependent of nitric oxide synthase (NOS) activation. Our results indicate that the abdominal acute application of PBM at 660nm is able to induce a long lasting hypotensive effect in hypertensive rats and vasodilation by a NO dependent mechanism.

Crystal structure of the human ubiquitin conjugating enzyme complex, hMms2-hUbc13.

The ubiquitin conjugating enzyme complex Mms2-Ubc13 plays a key role in post-replicative DNA repair in yeast and the NF-kappaB signal transduction pathway in humans. This complex assembles novel polyubiquitin chains onto yet uncharacterized protein targets. Here we report the crystal structure of a complex between hMms2 (Uev1) and hUbc13 at 1.85 A resolution and a structure of free hMms2 at 1.9 A resolution. These structures reveal that the hMms2 monomer undergoes a localized conformational change upon interaction with hUbc13. The nature of the interface provides a physical basis for the preference of Mms2 for Ubc13 as a partner over a variety of other structurally similar ubiquitin-conjugating enzymes. The structure of the hMms2-hUbc13 complex provides the conceptual foundation for understanding the mechanism of Lys 63 multiubiquitin chain assembly and for its interactions with the RING finger proteins Rad5 and Traf6.