Cytoglobin (CYGB), a new member of the globin family, was discovered in 2001 as a protein associated with stellate cell activation (stellate cell activation-associated protein [STAP]). Knowledge of CYGB, including its crystal, gene, and protein structures as well as its physiological and pathological importance, has increased progressively. We investigated the roles of oxygen (O2)-binding CYGB as STAP in hepatic stellate cells (HSCs) to understand the part played by this protein in their pathophysiological activities. Studies involving CYGB-gene-deleted mice have led us to suppose that CYGB functions as a regulator of O2 homeostasis; when O2 homeostasis is disrupted, HSCs are activated and play a key role(s) in hepatic fibrogenesis. In this review, we discuss the rationale for this hypothesis.
In plants, vascular stem cells continue to give rise to all xylem and phloem cells, which constitute the plant vascular system. During plant vascular development, the peptide, tracheary element differentiation inhibitory factor (TDIF), regulates vascular stem cell fate in a non-cell-autonomous fashion. TDIF promotes vascular stem cell proliferation through up-regulating the transcription factor gene WUS-related HOMEOBOX4, and it suppresses xylem differentiation from vascular stem cells through the activation of Glycogen Synthase Kinase 3 proteins. VASCULAR-RELATED NAC-DOMAIN6 and 7 (VND6 and 7) are master transcription factors, and ectopic expression of VND6 and VND7 in various plants induces differentiation of different types of cells into metaxylem and protoxylem tracheary elements, respectively. These genes up-regulate genes involved in both patterned secondary cell wall formation and programmed cell death to form tracheary elements. Secondary wall patterns are formed by localized deposition of cellulose microfibrils, which is guided by cortical microtubules. Local activation of the small G-protein, Rho-type 11 determines distribution of cortical microtubules.