Xiaoyan Lv

FLNA and PGK1 are Two Potential Markers for Progression in Hepatocellular Carcinoma

Background/Aims: Hepatocellular carcinoma (HCC) is one of the most deadly diseases; metastasis and recurrence are the most important factors that affect the therapy of HCC chronically. Until now, the prognosis for the metastasis of HCC had not improved. Recently, several proteins that are related to metastasis and invasion of HCC were identified, but the effective markers still remain to be elucidated. Methods: In this study, comparative proteomics was used to study the differentially expressed proteins in two HCC cell lines MHCC97L and HCCLM9, which have low and high metastatic potentials, respectively. Results: Our findings indicated that filamin A (FLNA) and phosphoglycerate kinase 1 (PGK1) were two significantly differentially expressed proteins, with high expression in HCCLM9 cells, and may influence the metastasis of HCC cells. Conclusion: Taken together with the confirmation of expression on the mRNA level, we propose the use of FLNA and PGK1 as potential markers for the progression of HCC.

Aquaporin-1 expression and angiogenesis in rabbit chronic myocardial ischemia is decreased by acetazolamide

Aquaporin-1 (AQP1) is a water channel protein expressed in endothelial and epithelial cells of many tissues, including the vasculature, where it serves to increase water permeability of the cell membrane. Prior studies have also reported that AQP1 plays a central role in tumor angiogenesis by promoting endothelial cell migration. To investigate whether AQP1 might also influence vascular angiogenesis in ischemic myocardium, the expression level of AQP1 for 21 days post myocardial infarction in rabbit hearts was observed. Aquaporin-1 mRNA and protein levels in day 3, and peaked on day 7 post surgery. This correlated well with the pattern of neovascularization and increased water content of infarct border tissue, and suggested that AQP1 may be involved in myocardial angiogenesis in response to ischemia injury. These AQP1-induced changes were tempered by acetazolamide, a carbonic anhydrase inhibitor, which acted by downregulating AQP1 expression. Acetazolamide treatment did not significantly affect the expression of vascular endothelial growth factor in the tissues studied. Our findings indicate a novel role for AQP1 in postnatal angiogenesis, which has implications in diverse pathophysiological conditions including wound healing, tumor metastasis, and organ regeneration.

Understanding the cleavage of inter- and intramolecular linkages in corncob residue for utilization of lignin to produce monophenols

The cleavage of inter- and intramolecular linkages is a crucial but complicated issue for isolation and depolymerization of lignin in lignocellulosic biomass to produce biofuel. Herein, a Na2CO3–H2O–tetrahydrofuran system was adopted for studying the cleavage of these linkages in corncob residue. Almost all ether, ester and hydrogen bonds between lignin and cellulose were broken by Na2CO3 at 140 °C, resulting in 94.6% dissolution of lignin, meanwhile the C–O bond in the β-O-4 linkage and the Cα–Cβ bond in the aliphatic side-chain of lignin could be broken to obtain aryl aldehydes. At 300 °C, the CAr–Cα bond could be broken down, bringing about high selectivity to monophenols without substituted alkyl groups, and the total yield of monophenols reached up to 26.9 wt% without additional hydrogen. Na2CO3 could also inhibit the formation of a Cα-oxidized side-chain product and the elimination reaction of an –OH group on Cα forming p-coumaric acid. G and H units in the corncob residue were mostly connected by a β-O-4 linkage, whereas S units were possibly linked by an α-O-4 linkage. The hydrogen bonds at –OCH3 groups in S and G units in lignin could be disrupted by Na2CO3 to facilitate the dissolution and degradation of lignin.

Overexpression of FoxO1 Causes Proliferation of Cultured Pancreatic β Cells Exposed to Low Nutrition

Multiple lines of evidence have shown that the functional defect of pancreatic beta cells is the root cause of type 2 diabetes. FoxO1, a key transcription factor of fundamental cellular physiology and functions, has been implicated in this process. However, the underlying molecular mechanism is still largely unknown. Here, we show that the overexpression of FoxO1 promotes the proliferation of cultured pancreatic beta cells exposed to low nutrition, while no change in apoptosis was observed compared with the control group. Moreover, by using two specific inhibitors for PI3K and MAPK signaling, we found that FoxO1 might be the downstream transcription factor of these two pathways. Furthermore, a luciferase assay demonstrated that FoxO1 could regulate the expression of Ccnd1 at the transcription level. Collectively, our findings indicated that FoxO1 modulated by both MAPK and PI3K signaling pathways was prone to cause the proliferation, but not the apoptosis, of pancreatic beta cells exposed to low nutrition, at least partially, by regulating the expression of Ccnd1 at the transcription level.

A Modified TALEN-Based Strategy for Rapidly and Efficiently Generating Knockout Mice for Kidney Development Studies

The transcription activator-like effector nucleases (TALENs) strategy has been widely used to delete and mutate genes in vitro. This strategy has begun to be used for in vivo systemic gene manipulation, but not in an organ-specific manner. In this study, we developed a modified, highly efficient TALEN strategy using a dual-fluorescence reporter. We used this modified strategy and, within 5 weeks, we successfully generated kidney proximal tubule-specific gene Ttc36 homozygous knockout mice. Unilateral nephrectomy was performed on the 6-week-old founders (F0) to identify the knockout genotype prior to the birth of the offspring. This strategy was found to have little effect on reproduction in the knockout mice and inheritability of the knockout genotypes. The modified TALEN knockout strategy in combination with unilateral nephrectomy can be readily used for studies of gene function in kidney development and diseases.

Overexpression of Trpp5 contributes to cell proliferation and apoptosis probably through involving calcium homeostasis

Trpp5 is one member of the polycystic kidney disease (PKD) family, which belongs to transient receptor potential (TRP) superfamily. Our previous study has shown that Trpp5 is developmentally expressed in mouse testis and overexpression of Trpp5 increases intracellular free calcium concentration in MDCK cells. However, the roles of this protein in cellular processes are largely unknown. Here, we demonstrated that Trpp5 resided in both cytoplasm and cell membrane of HEK293 cells. We found that overexpression of Trpp5 slightly increased the calcium current amplitude of HEK293 cells and shifted the reversal potential to a more negative value. Meanwhile, overexpression of Trpp5 suppressed proliferation of Hela cells via inhibiting DNA replication and induced apoptosis of Hela cells with morphological changes and accumulation of fragmented DNA. Collectively, these findings suggest that Trpp5 might involve calcium homeostasis contributing to cell proliferation and apoptosis.

miR181c promotes apoptosis and suppresses proliferation of metanephric mesenchyme cells by targeting Six2 in vitro

Increasingly recognized importance has been assumed for microRNA (miRNA) in the regulation of the delicate balance of gene expression. In our study, we aimed to explore the regulation role of miR181c towards Six2 in metanephric mesenchyme (MM) cells.

Xenopus Dbx2 is involved in primary neurogenesis and early neural plate patterning

The evolutionarily conserved Dbx homeodomain-containing proteins play important roles in the development of vertebrate central nervous system. In mouse, Dbx and Nkx6 have been suggested to be cross-repressive partners involved in the patterning of ventral neural tube. Here, we have isolated Xenopus Dbx2 and studied its developmental expression and function during neural development. Like XDbx1, from mid-neurula stage on, XDbx2 is expressed in stripes between the primary motoneurons and interneurons. At the tailbud stages, it is detected in the middle region of the neural tube. XDbx2 acts as a transcriptional repressor in vitro and over-expression of XDbx2 inhibits primary neurogenesis in Xenopus embryos. Over-expression of XDbx genes represses the expression of XNkx6.2 and vise versa. Knockdown of either XDbx1, XDbx2 or both by specific morpholinos induces lateral expansion of XNkx6.2 expression domains. These data reveal conserved roles for Dbx in primary neurogenesis and dorsoventral neural patterning in Xenopus.

Overexpression of JKTBP1 induces androgen-independent LNCaP cell proliferation through activation of epidermal growth factor-receptor (EGF-R).

Heterogenous nuclear ribonucleoprotein D‐like protein (JKTBP) belongs to a new member of hnRNPs. Previous studies implied that JKTBP1 may be associated with the progression of androgen‐independent (AI) prostate cancer. In this study, we generated three stable LNCaP cell lines which expressed exogenous JKTBP1. Furthermore, the effect of ectopic JKTBP1 on the proliferation of LNCaP cells and its mechanism was investigated. We originally found that the ectopic JKTBP1 expression resulted in the proliferation of LNCaP cells in an AI way, as well as inducing the upregulated expression of EGF‐R and prostate‐specific antigen (PSA), but did not influence the expression level of AR. Moreover, AG1478 suppressed the effect of proliferation induced by JKTBP1. In addition, immunohistochemistry showed that JKTBP1 expression was significantly elevated in AI prostate cancer tissues when compared with the androgen‐dependent (AD) prostate cancer and benign prostatic hyperplasia. Our data indicated that overexpression of JKTBP1 in LNCaP cells leads to abnormal cell proliferation and may be involved in the process of AD to AI through induction of EGF‐R expression. Copyright

Giant, mutilating facial lupus vulgaris due to long-term misdiagnosis

A 54‐year‐old farmer presented with a 42‐year history of a non‐healing mutilating plaque on his face which was triggered by trauma. At presentation, he had a well‐marginated, large, dark red plaque, predominantly involving the left side of his face with overlying telangiectases, scaling and scarring, predominantly involving the left side of his face [Figure 1]. The left eyebrow was sparse, he had left‐sided facial paralysis and could not shut his left eye. Both eyes showed conjunctival congestion and decreased visual acuity. The nasal bridge was collapsed with bilateral nasal atrophy and most of the left pinna had disappeared. He had lost his hearing in the left ear 14 years earlier. He had been diagnosed to have conjunctivitis, otitis media and facial dermatitis at various local hospitals but the suggested treatments did not work. He had no other illnesses or any known contact with tuberculosis.