The subfamily Xerocomoideae (Boletaceae, Boletales) in China.

Xerocomoideae is an ecologically and economically important Boletaceae subfamily (Boletales) comprising 10 genera. Although many studies have focused on Xerocomoideae in China, the diversity, taxonomy and molecular phylogeny still remained incompletely understood. In the present study, taxonomic and phylogenetic studies on Chinese species of Xerocomoideae were carried out by morphological examinations and molecular phylogenetic analyses. Eight genera in Xerocomoideae, viz. Aureoboletus, Boletellus, Heimioporus, Hemileccinum, Hourangia, Phylloporus, Pulchroboletus, and Xerocomus were confirmed to be distributed in China; 97 species of the subfamily were accepted as being distributed in China; one ambiguous taxon was tentatively named Bol. aff. putuoensis; two synonyms, viz. A. marroninus and P. dimorphus were defined. Among the Chinese accepted species, 13 were newly described, viz. A. albipes, A. conicus, A. ornatipes, Bol. erythrolepis, Bol. rubidus, Bol. sinochrysenteroides, Bol. subglobosus, Bol. zenghuoxingii, H. squamipes, P. hainanensis, Pul. erubescens, X. albotomentosus, and X. fuscatus, 36 known species were redescribed, and the other 48 species were reviewed. Keys to accepted species of Aureoboletus, Boletellus, Heimioporus, Hemileccinum, Hourangia, Phylloporus, and Xerocomus in China were also provided. Taxonomic novelties: New species: Aureoboletus albipes N.K. Zeng, Xu Zhang & Zhi Q. Liang, A. conicus N.K. Zeng, Xu Zhang & Zhi Q. Liang, A. ornatipes N.K. Zeng, Xu Zhang & Zhi Q. Liang, Boletellus erythrolepis N.K. Zeng, R. Xue, S. Jiang & Zhi Q. Liang, Bol. rubidus N.K. Zeng, R. Xue, Y.J. Hao & Zhi Q. Liang, Bol. sinochrysenteroides N.K. Zeng, R. Xue & Kuan Zhao, Bol. subglobosus N.K. Zeng, R. Xue, S. Jiang & Zhi Q. Liang, Bol. zenghuoxingii N.K. Zeng, R. Xue, S. Jiang & Zhi Q. Liang, Hemileccinum squamipes N.K. Zeng, Chang Xu & Zhi Q. Liang, Phylloporus hainanensis N.K. Zeng, L.L. Wu, & Zhi Q. Liang, Pulchroboletus erubescens N.K. Zeng, Chang Xu & Zhi Q. Liang, Xerocomus albotomentosus N.K. Zeng, H.J. Xie, Chang Xu & Zhi Q. Liang, and X. fuscatus N.K. Zeng, H.J. Xie, Chang Xu & Zhi Q. Liang. Citation: Xue R, Zhang X, Xu C, Xie HJ, Wu LL, Wang Y, Tang LP, Hao YJ, Zhao K, Jiang S, Li Y, Yang YY, Li Z, Liang ZQ, Zeng NK (2023). The subfamily Xerocomoideae (Boletaceae, Boletales) in China. Studies in Mycology 106: 95-197. doi: 10.3114/sim.2022.106.03.

LncRNA TUG1 promotes osteoarthritis-induced degradation of chondrocyte extracellular matrix via miR-195/MMP-13 axis.

OBJECTIVE: Osteoarthritis is a degenerative disease characterized by articular cartilage degradation. Long non-coding ribonucleic acid (lncRNA) plays important roles in a series of biological processes, but its role in osteoarthritis is still not quite clear. This study aims to investigate the regulatory role of taurine upregulated gene 1 (TUG1) in osteoarthritis. PATIENTS AND METHODS: The expression level of lncRNA-TUG1 in cartilages of patients with osteoarthritis and those of normal people was compared using Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Primary chondrocytes were induced by interleukin-1 beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α), followed by expression detection of lncRNA-TUG1, microRNA-195 (miR-195), and matrix metalloproteinase-13 (MMP-13). In addition, in vitro regulatory roles of lncRNA-TUG1 and miR-195 in osteoarthritis were verified by transfection of lncRNA-TUG1 and miR-195 plasmids. The dimethylmethylene blue (DMMB) assay was performed to analyze the secretion and formation of soluble sulfated glycosaminoglycan (sGAG). RESULTS: The expression levels of lncRNA-TUG1 and MMP-13 in cartilages of patients with osteoarthritis were higher than those in cartilages of normal people, while the level of miR-195 decreased in cartilages of patients with osteoarthritis. After chondrocytes were induced by IL-1ß and TNF-α, the expression of lncRNA-TUG1 increased. Overexpression of lncRNA-TUG1 decreased the expressions of miR-195, collagen, and aggrecan, but increased the expression of MMP-13. LncRNA-TUG1 knockdown obtained the opposite results. CONCLUSIONS: LncRNA-TUG1 regulates the degradation of extracellular matrix in osteoarthritis via lncRNA-TUG1/miR-195/MMP-13 axis.

Characteristics of cathelicidin-Bg, a novel gene expressed in the ear-side gland of Bufo gargarizans.

The traditional Chinese medicine Chan Su (toad venom) comprises dried secretions of the ear-side gland of Bufo gargarizans. Chan Su is known for its small molecular components, which include telocinobufagin, marinobufagin, and bufalin, while in other amphibians, studies mainly focus on peptide components. Until recently, no genes expressed in the ear-side gland of B. gargarizans gland had been cloned. In this study, cathelicidin-Bg, a coding sequence of anti-microbial peptide (AMP), was cloned. The predicted amino acid sequence of cathelicidin-Bg was very similar to that from other amphibians, with a 34-amino acid mature peptide predicted in the C-terminus. The functions of this mature peptide were verified by microbe and tumor cell inhibition assays. Our results showed that the mature peptide of cathelicidin-Bg could inhibit the proliferation of Staphylococcus aureus and Pseudomonas aeruginosa. The mature peptide was also shown to selectively inhibit tumor cells. These results indicate that the identified coding sequence represents an active peptide of Chan Su.

Genistein-induced apoptosis is mediated by endoplasmic reticulum stress in cervical cancer cells.

OBJECTIVE: Genistein, a major isoflavone found in soybeans, exhibits anti-cancer activity. Endoplasmic reticulum (ER) stress is known to be implicated in apoptosis induced by anti-cancer drugs. This study aimed to characterize the role of ER stress in genistein-induced apoptosis in cervical cancer. MATERIALS AND METHODS: HeLa cells were treated with genistein or/and 4-phenylbutyric acid. Cell viability and apoptosis were evaluated by MTT assay and flow cytometry. Protein levels were detected by Western blot analysis. RESULTS: Genistein suppressed the viability of HeLa cells in a dose dependent manner. In addition, genistein caused apoptosis in HeLa cells in a dose dependent manner. Genistein triggered ER stress in HeLa cells, as indicated by the upregulation of glucose-regulated protein 78 (GRP78) and CHOP expression. Furthermore, ER stress inhibitor 4-phenylbutyric acid alleviated genistein-induced apoptosis and ER stress in HeLa cells. CONCLUSIONS: Our results suggest that ER stress contributes to genistein-induced apoptosis in cervical cancer cells, and genistein is a promising agent for cervical cancer therapy.

IL-1 beta inhibits IFN-gamma-induced class II MHC expression by suppressing transcription of the class II transactivator gene.

Class II MHC Ags are critical for the initiation of immune responses by presenting Ag to T lymphocytes, leading to their activation and differentiation. The transcriptional activation of class II MHC genes requires the induction of the class II transactivator (CIITA) protein, a master regulator that is essential for both constitutive and IFN-gamma-inducible class II MHC expression. The cytokine IL-1beta has been shown to inhibit IFN-gamma-induced class II MHC expression in various cell types. We investigated the underlying mechanism of this inhibitory effect of IL-1beta using human astroglioma cell lines. Our findings demonstrate that IL-1beta prevents the expression of class II MHC mRNA and protein upon treatment with IFN-gamma. Furthermore, we demonstrate that IFN-gamma induction of CIITA mRNA expression is inhibited by treatment of cells with IL-1beta. IL-1beta suppressed IFN-gamma activation of the type IV CIITA promoter in astroglioma cells, indicating that the inhibitory influence of IL-1beta is mediated by inhibition of CIITA transcription. IL-1beta did not interfere with IFN-gamma receptor signal transduction, since tyrosine phosphorylation, nuclear translocation, and DNA binding of STAT-1alpha to an IFN-gamma activation sequence of the type IV CIITA promoter were not affected by IL-1beta. As well, IL-1beta treatment did not affect the ability of IFN-gamma-induced interferon-regulatory factor-1 (IRF-1) to bind the IRF-1 element within the type IV CIITA promoter. This study suggests that IL-1beta may play a role in regulating immunoreactivity by inhibiting transcription of the CIITA gene, thereby reducing subsequent class II MHC expression.

HIV glycoprotein 120 enhances intercellular adhesion molecule-1 gene expression in glial cells. Involvement of Janus kinase/signal transducer and activator of transcription and protein kinase C signaling pathways.

It is well established that the two major glial cells in the central nervous system (CNS), astrocytes and microglia, are key participants in mediating the neurologic dysfunction associated with HIV infection of the CNS. In this study, we investigated the ability of the major envelope glycoprotein of HIV, glycoprotein 120 (gp120), to regulate intercellular adhesion molecule-1 (ICAM-1) expression in glial cells, because ICAM-1 is important in mediating immune responsiveness in the CNS, facilitating entry of HIV-infected cells into the CNS, and promoting syncytia formation. Our results indicate that gp120 enhances ICAM-1 gene expression in primary rat astrocytes, primary human astrocytes, a human astroglioma cell line CRT, and primary rat microglia. The signal transduction events involved in gp120-mediated enhancement of ICAM-1 appear to involve activation of both protein kinase C and tyrosine kinase, because inhibitors of protein kinase C and tyrosine kinase abrogate gp120-mediated ICAM-1 expression in both astrocytes and microglia. Moreover, gp120 induces tyrosine phosphorylation of signal transducer and activator of transcription (STAT-1 alpha) as well as the Janus kinase (JAK2) in glial cells. We also demonstrate that gp120-mediated ICAM-1 expression has functional significance, as it enhances the ability of monocytic cells to bind to gp120-stimulated human astrocytes in an ICAM-1/beta 2 integrin-dependent fashion. These results provide new insights into how gp120 can influence the involvement of glial cells in the pathogenesis of AIDS dementia complex.

Differential regulation of astrocyte TNF-alpha expression by the cytokines TGF-beta, IL-6 and IL-10.

In this study, we demonstrate that transforming growth factor-beta (TGF-beta), interleukin-10 (IL-10) and interleukin-6 (IL-6) inhibit tumor necrosis factor-alpha expression by primary rat astrocytes. Treatment of astrocytes with TGF-beta alone had no effect on TNF-alpha expression, however, TGF-beta suppressed induction of TNF-alpha expression at both the protein and mRNA level. In contrast, IL-10 and IL-6 both inhibited TNF-alpha protein expression by astrocytes, but had no effect on mRNA levels. The extent of IL-6-mediated inhibition was greatest when astrocytes were pretreated with IL-6 for 12-24 hr, then exposed to the inducing stimuli, while IL-10 was an effective inhibitor even when added simultaneously with the inducing stimuli. Collectively, these data indicate that TGF-beta, IL-6 and IL-10 are all capable of inhibiting TNF-alpha expression by astrocytes, although these immunosuppressive cytokines act at different levels of gene expression; i.e. TGF-beta at the transcriptional level and IL-10/IL-6 at the translational level. These results indicate that TGF-beta, IL-6 and IL-10 are important regulators of cytokine production by astrocytes under inflammatory conditions in the brain, and can contribute to controlling the production of detrimental cytokines such as TNF-alpha.

Differential modulation of astrocyte cytokine gene expression by TGF-beta.

In this study, we demonstrate that TGF-beta inhibits TNF-alpha expression, and induces/enhances IL-6 expression by primary rat astrocytes. Treatment of astrocytes with TGF-beta alone had no effect on TNF-alpha mRNA or protein expression; however, TGF-beta suppressed induction of TNF-alpha expression by three different stimuli (IFN-gamma/LPS, IFN-gamma/IL-1 beta, TNF-alpha) at both the protein and mRNA level. The extent of TGF-beta-mediated inhibition was greatest when astrocytes were pretreated with TGF-beta for 6 to 24 h, then exposed to the inducing stimuli. Inhibition of TNF-alpha mRNA steady-state levels by TGF-beta was a result of inhibition of TNF-alpha gene transcription, rather than degradation of the TNF-alpha message. In contrast, TGF-beta alone induced expression of IL-6 by astrocytes and synergized with two other cytokines, IL-1 beta and TNF-alpha, for enhanced IL-6 expression. TGF-beta-induced/enhanced IL-6 expression was mediated by transcriptional activation of the IL-6 gene. These results indicate that TGF-beta is an important regulator of cytokine production by astrocytes under inflammatory conditions in the brain.

Signal transduction pathways mediating astrocyte IL-6 induction by IL-1 beta and tumor necrosis factor-alpha.

One immune function of astrocytes is IL-6 production. Synthesis of IL-6 within the central nervous system (CNS) can produce several different responses, acting on glia, neurons, and lymphocytes infiltrating brain tissue, and some of these effects are associated with CNS autoimmune disease. IL-6 gene expression in astrocytes is regulated by cytokines, infectious agents, neuropeptides, and neurotransmitters, and most of these stimuli interact synergistically. To examine the integration of these diverse factors in the control of IL-6 production, we have studied the involvement of underlying signal transduction processes using neonatal rat astrocytes. We have focused on signal transduction related to the stimulation of IL-6 gene expression by IL-1 beta and TNF-alpha. Our results indicate that stimuli related to protein kinase C (PKC), such as PMA and calcium ionophore A23187, increase IL-6 expression, whereas pharmacologic inhibitors of PKC inhibit IL-6 induction by IL-1 beta and TNF-alpha. Furthermore, both IL-1 beta and TNF-alpha stimulate PKC activity in astrocytes. Stimulators of the cAMP pathway, such as cholera toxin, forskolin, and dibutyryl cAMP, also induced astrocyte IL-6 gene expression. However, inhibition of the cAMP pathway effector, protein kinase A, did not reduce the induction of astrocyte IL-6 gene expression in response to IL-1 beta or TNF-alpha, and an ELISA for cAMP detected only very small increases in cAMP synthesis in response to these cytokines. These data suggest that although cAMP does activate astrocyte IL-6 gene expression, it is the PKC pathway that plays a primary role in the stimulation of astrocyte IL-6 gene expression by IL-1 beta and TNF-alpha.