RhoA GTPase plays a variety of functions in regulation of cytoskeletal proteins, cellular morphology, and migration along with various proliferation and transcriptional activity in cells. RhoA activity is regulated by guanine nucleotide exchange factors (GEFs), GTPase activating proteins (GAPs), and the guanine nucleotide dissociation factor (GDI). The RhoA-RhoGDI complex exists in the cytosol and the active GTP-bound form of RhoA is located to the membrane. GDI displacement factors (GDFs) including IκB kinase γ (IKKγ) dissociate the RhoA-GDI complex, allowing activation of RhoA through GEFs. In addition, modifications of Tyr42 phosphorylation and Cys16/20 oxidation in RhoA and Tyr156 phosphorylation and oxidation of RhoGDI promote the dissociation of the RhoA-RhoGDI complex. The expression of RhoA is regulated through transcriptional factors such as c-Myc, HIF-1α/2α, Stat 6, and NF-κB along with several reported microRNAs. As the role of RhoA in regulating actin-filament formation and myosin-actin interaction has been well described, in this review we focus on the transcriptional activity of RhoA and also the regulation of RhoA message itself. Of interest, in the cytosol, activated RhoA induces transcriptional changes through filamentous actin (F-actin)-dependent ("actin switch") or-independent means. RhoA regulates the activity of several transcription regulators such as serum response factor (SRF)/MAL, AP-1, NF-κB, YAP/TAZ, β-catenin, and hypoxia inducible factor (HIF)-1α. Interestingly, RhoA also itself is localized to the nucleus by an as-yet-undiscovered mechanism.

Summary In suspension bridges, hanger cables are the main load‐supporting members. The tension of the hanger cables of a suspension bridge is a very important parameter for assessing the integrity and safety of the bridge. In general, indirect methods are used to measure the tension of the hanger cables of a suspension bridge in use. A representative indirect method is the vibration method, which extracts modal frequencies from the cables' responses and then measures the cable tension using the cables' geometric conditions and the modal frequencies. In this study, ambient vibration tests were conducted on a suspension bridge in use to verify the validity of the image‐based back analysis method, which can estimate the tension of remote hanger cables using the modal frequencies as a parameter. The tension estimated through back analysis, which was conducted to minimize the difference between the modal frequencies calculated using finite element analysis of the hanger cables and the measured modal frequencies, was compared with that measured using the vibration method. It was confirmed that reliable tension estimation is possible even with low‐order modal frequencies when the image‐based back analysis method is used.

Although the migration of hepatic stellate cells (HSCs) is important for hepatic fibrosis, the regulation of this migration is poorly understood. Notably, transforming growth factor (TGF)-β1 induces monocyte migration to sites of injury or inflammation during the early phase, but inhibits cell migration during the late phase. In the present study, the role of transforming protein RhoA signaling in TGF-β1-induced HSC migration was investigated. TGF-β1 was found to increase the protein and mRNA levels of smooth muscle actin and collagen type I in HSC-T6 cells. The level of RhoA-GTP in TGF-β1-stimulated cells was significantly higher than that in control cells. Furthermore, the phosphorylation of cofilin and formation of filamentous actin (F-actin) were more marked in TGF-β1-stimulated cells than in control cells. Additionally, TGF-β1 induced the activation of nuclear factor-κB, and the expression of extracellular matrix proteins and several cytokines in HSC-T6 cells. The active form of Rap1 (Rap1 V12) suppressed RhoA-GTP levels, whereas the dominant-negative form of Rap1 (Rap1 N17) augmented RhoA-GTP levels. Therefore, the data confirmed that Rap1 regulated the activation of RhoA in TGF-β1-stimulated HSC-T6 cells. These findings suggest that TGF-β1 regulates Rap1, resulting in the suppression of RhoA, activation of and formation of F-actin during the migration of HSCs.

Rho guanine nucleotide exchange factor (RhoGEF) regulates various cellular processes including cell polarity, cytokinesis, and cell movements via activating small GTPase such as RhoA, Rac1 and CDC42. During gastrulation of Xenopus embryos, noncanonical Wnt signaling is the major signal pathway to regulate convergent and extension cell movements in DMZ region. In previous publications, activin induces dorsal mesoderm and noncanonical Wnt signaling is highly activated in dorsal mesoderm to promote cell movements. Although about 70 GEF distinct GEF homologues have been studied in humans, few GEFs of Xenopus are only identified and explored for its function during early embryogenesis.In this study, we showed that EST gene (assesion No. XL.3374), which has been named xARHGEF3.2 was induced by activin treatment in ectodermal explants and expressed at dorsal marginal region in gastrula embryo. It was constructed to explore the role of xARHGEF3.2 during gastrulation. Over‐expression / knockdown of ARHGEF3.2 caused gastrulation defects. Furthermore, Biochemical analysis showed that xARHGEF3.2 activated RhoA through interaction with Dishevelled and Daam‐1.Taken together, our results suggest that xARHGEF3.2 is induced by activin signaling and modulates convergent and extension cell movement via Wnt‐PCP signaling during the early Xenopus embryos development