This article reviews the main events of embryo-implantation and decidualization in rodents. In common laboratory rodents the embryo attaches to the uterine epithelial lining, usually on days 4 to 6 of pregnancy. A progressive degree of proximity between trophoblast and epithelium occurs until the epithelial cells undergo apoptosis and detach from the basement membrane. During the attachment stage, the spindle-shaped connective tissue cells that underlie the epithelium next to the embryos transform into polyhedral and closely packed decidual cells. Following the epithelial detachment and the breaching of the basement membrane the embryo is thus in direct contact with decidual cells. These cells accumulate organelles associated with synthesis of macro-molecules, intermediate filaments, and eventually lipid droplets and glycogen. Another remarkable feature of decidual cells is the establishment of gap and adherens intercellular junctions. Differentiation of fibroblasts into decidual cells advances antimesometrially and mesometrially, creating in the endometrium several regions of cells with different morphology. The whole phenomenon of decidualization which is normally triggered by the embryo can be artificially induced in pseudo-pregnant or hormonally-prepared animals with the use of diverse stimuli. The uterine epithelium is probably responsible for the transduction of the initial stimulus. Prostaglandins have been shown to be important in the induction of decidualization. More recently other substances such as leukotrienes, platelet-activating factor (PAF), and transforming growth factor (TGF) have been thought to play a role in induction. Much evidence points to prostaglandin production by the decidual cells. New proteins such as a luteotropic factor, desmin, and other molecules were shown to be produced after rat stromal cells undergo decidual transformation. The extracellular matrix of the mouse decidua contains very thick collagen fibrils. Mouse decidual cells are also very active in phagocytosing the thick fibrils, contributing to the remodeling and involution of the decidua that accompanies embryonic growth. Radioautographic data indicates that mouse decidual cells produce and secrete collagen and sulfated proteoglycans.

The results suggest that low-intensity training can significantly reduce pressure in SHR while normalizing both the arteriole morphology and the resistance of the skeletal muscle microcirculation.

Evidence demonstrates that sympathetic nervous system (SNS) activation causes osteopenia via b 2 -adrenoceptor (b2-AR) signaling. Here we show that female mice with chronic sympathetic hyperactivity owing to double knockout of adrenoceptors that negatively regulate norepinephrine release, a 2A -AR and a 2C -AR (a 2A /a 2C -ARKO), present an unexpected and generalized phenotype of high bone mass with decreased bone resorption and increased formation. In a 2A /a 2C -ARKO versus wild-type (WT) mice, micro-computed tomographic (mCT) analysis showed increased, better connected, and more plate-shaped trabeculae in the femur and vertebra and increased cortical thickness in the vertebra, whereas biomechanical analysis showed increased tibial and femoral strength. Tibial mRNA expression of tartrate-resistant acid phosphatase (TRACP) and receptor activator of NF-kB (RANK), which are osteoclast-related factors, was lower in knockout (KO) mice. Plasma leptin and brain mRNA levels of cocaine amphetamine-regulated transcript (CART), which are factors that centrally affect bone turnover, and serum levels of estradiol were similar between mice strains. Tibial b 2 -AR mRNA expression also was similar in KO and WT littermates, whereas a 2A -, a 2B -and a 2C -AR mRNAs were detected in the tibia of WT mice and in osteoblast-like MC3T3-E1 cells. By immunohistochemistry, we detected a 2A -, a 2B -, a 2C -and b 2 -ARs in osteoblasts, osteoclasts, and chondrocytes of 18.5-day-old mouse fetuses and 35-day-old mice. Finally, we showed that isolated osteoclasts in culture are responsive to the selective a 2 -AR agonist clonidine and to the nonspecific a-AR antagonist phentolamine. These findings suggest that b 2 -AR is not the single adrenoceptor involved in bone turnover regulation and show that a 2 -AR signaling also may mediate the SNS actions in the skeleton. ß

The results suggest that increased venule density is a specific adaptation of SHR skeletal muscle to training. Venular growth may contribute to both the pressure-lowering effect and the large HLF at high exercise intensities observed in the trained SHR.

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