Actin remodeling mediates ROS production and JNK activation to drive apoptosis-induced proliferation.

Stress-induced cell death, mainly apoptosis, and its subsequent tissue repair is interlinked although our knowledge of this connection is still very limited. An intriguing finding is apoptosis-induced proliferation (AiP), an evolutionary conserved mechanism employed by apoptotic cells to trigger compensatory proliferation of their neighboring cells. Studies using Drosophila as a model organism have revealed that apoptotic caspases and c-Jun N-terminal kinase (JNK) signaling play critical roles to activate AiP. For example, the initiator caspase Dronc, the caspase-9 ortholog in Drosophila, promotes activation of JNK leading to release of mitogenic signals and AiP. Recent studies further revealed that Dronc relocates to the cell cortex via Myo1D, an unconventional myosin, and stimulates production of reactive oxygen species (ROS) to trigger AiP. During this process, ROS can attract hemocytes, the Drosophila macrophages, which further amplify JNK signaling cell non-autonomously. However, the intrinsic components connecting Dronc, ROS and JNK within the stressed signal-producing cells remain elusive. Here, we identified LIM domain kinase 1 (LIMK1), a kinase promoting cellular F-actin polymerization, as a novel regulator of AiP. F-actin accumulates in a Dronc-dependent manner in response to apoptotic stress. Suppression of F-actin polymerization in stressed cells by knocking down LIMK1 or expressing Cofilin, an inhibitor of F-actin elongation, blocks ROS production and JNK activation, hence AiP. Furthermore, Dronc and LIMK1 genetically interact. Co-expression of Dronc and LIMK1 drives F-actin accumulation, ROS production and JNK activation. Interestingly, these synergistic effects between Dronc and LIMK1 depend on Myo1D. Therefore, F-actin remodeling plays an important role mediating caspase-driven ROS production and JNK activation in the process of AiP.

Protective effects of cinnamon powder against hyperlipidemia and hepatotoxicity in butter fed female albino mice.

A butter-enriched high-fat diet changes lipid metabolism, resulting in fat storage, hyperlipidemia and obesity. Effects of cinnamon powder were investigated in butter-fed mice. 40 Swiss Albino mice, aged 28 to 30 days, were randomly assigned into two groups. Group A was an untreated control group (n = 8) and another group (n = 32) was a butter-treated group fed 10% butter. In the fifth week, mice of the butter-fed group were further divided into four equal groups: B, C, D, and E (n = 8), fed 10% butter with cinnamon 200 mg, 400 mg, and 600 mg powder per liter drinking water, respectively for 10 weeks. The butter-fed group was gained the most weight. Cinnamon supplementation significantly normalized weight gain and had no harmful effects on hematological parameters. Butter supplementation significantly increased total cholesterol (TC), triglycerides, and LDL cholesterol (LDL-c) whereas, cinnamon powder significantly reduced TC, LDL-c and glucose levels. In butter-fed mice, a significant increase was observed in the liver enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels with subsequent fat deposition in the liver. Excitingly, these enzymes were decreased and no fat depositions were observed in the liver of cinnamon-treated mice. Applying different concentrations of cinnamon powder improved the lipid profile in butter-fed female albino mice.

Impacts of stocking density rates on welfare, growth, and hemato-biochemical profile in broiler chickens.

OBJECTIVE: The study investigated the effect of different stocking density (SD) rates on the welfare, growth, and hemato-biochemical parameters in broiler chickens. MATERIALS AND METHODS: 106 broiler chicks of 10 days old were used and assigned into four groups: A, B, C, and D. The chicks of group A were reared in floor space containing one bird per square foot area (SD1.0). The chicks of groups B, C, and D were reared at 1.5, 2.0, and 2.5 birds per square foot area (SD1.5, SD2.0, and SD2.5). Welfare, body weight, and hemato-biochemical parameters were assessed and monitored by physical observation and laboratory methods. RESULTS: The birds reared at SD2.0, and SD2.5 rates showed increased panting breathing. Wet feces adhered below the vent. There were a significant number of birds showing dirtiness of body and feathers. Birds reared in SD2.5 were familiar with moist litters and high ammonia smell. Foot-pad dermatitis, scratches, and blister formation were detected in the leg. The study revealed that the higher SD negatively correlated to the welfare behavior indicators. Live body weight was significantly (p < 0.05) decreased in birds reared at higher SD rates. Birds housed in SD1.0 and SD1.5 are optimum for body weight and improved feed conversion ratio. The hemato-biochemical parameters of birds reared at various SD rates did not differ. The total leucocyte count increased significantly, while total serum proteins decreased gradually as SD rates increased. CONCLUSION: This work explores that higher SD negatively affects welfare and growth performance in broiler chickens.