Periodontitis and other bone loss diseases, decreasing bone volume and strength, have a significant impact on millions of people with the risk of tooth loss and bone fracture. The integrity and strength of bone are maintained through the balance between bone resorption and bone formation by osteoclasts and osteoblasts, respectively, so the loss of bone results from the disruption of such balance due to increased resorption or/and decreased formation of bone. The goal of therapies for diseases of bone loss is to reduce bone loss, improve bone formation, and then keep healthy bone density. Current therapies have mostly relied on long-term medication, exercise, anti-inflammatory therapies, and changing of the life style. However there are some limitations for some patients in the effective treatments for bone loss diseases because of the complexity of bone loss. Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine, and recent studies have indicated that IL-10 can contribute to the maintenance of bone mass through inhibition of osteoclastic bone resorption and regulation of osteoblastic bone formation. This paper will provide a brief overview of the role of IL-10 in bone loss diseases and discuss the possibility of IL-10 adoption in therapy of bone loss diseases therapy.

Tumor microenvironment (TME) plays an active role in promoting tumor progression. To further understand the communication between TME and tumor cells, this study aimed at investigating the involvement of CD44, a type I cell surface receptor, in the crosstalk between tumor cells and TME. We have previously shown that chondroitin sulfate proteoglycan serglycin (SRGN), a CD44-interacting factor, was preferentially secreted by cancer-associated fibroblasts (CAFs) for promoting tumor growth in breast cancer patients. In this study, we show that SRGN is overexpressed in primary non-small cell lung cancers (NSCLCs), by both carcinoma and stromal cells. Using gain-of-function and loss-of-function approaches, we show that SRGN promotes NSCLC cell migration and invasion as well as colonization in the lung and liver in a CD44-dependent manner. SRGN induces lung cancer cell stemness, as demonstrated by its ability to enhance NSCLC cell sphere formation via Nanog induction, accompanied with increased chemoresistance and anoikis-resistance. SRGN promotes epithelial-mesenchymal transition by enhancing vimentin expression via CD44/NF-κB/claudin-1 (CLDN1) axis. In support, CLDN1 and SRGN expression are tightly linked together in primary NSCLC. Most importantly, increased expression of SRGN and/or CLDN1 predicts poor prognosis in primary lung adenocarcinomas. In summary, we demonstrate that SRGN secreted by tumor cells and stromal components in the TME promotes malignant phenotypes through interacting with tumor cell receptor CD44, suggesting that a combined therapy targeting both CD44 and its ligands in the TME may be an attractive approach for cancer therapy.

Arabidopsis transcriptional factors LEAFY COTYLEDON1 (LEC1), LEAFY COTYLEDON2 (LEC2), FUSCA3 (FUS3), ABSCISIC ACID3 (ABI3), and ABSCISIC ACID5 (ABI5) are known to regulate multiple aspects of seed development. In an attempt to understand the developmental control of storage product accumulation, we observed the expression time course of the five transcripts. The sequential expression of these factors during seed fill suggests differentiation of their normal responsibilities. By extending the expression periods of the two early genes LEC1 and LEC2 in transgenic seeds, we demonstrated that the subsequent timing of FUS3, ABI3, and ABI5 transcripts depends on LEC1 and LEC2. Because a delayed onset or reduced level of FUS3 mRNA coincided with reduction of seed oil content in the transgenic seeds, the role of FUS3 in oil deposition was further examined. Analysis of published seed transcriptome data indicated that FUS3 transcript increased together with nearly all the plastidial fatty acid biosynthetic transcripts during development. The ability of FUS3 to rapidly induce fatty acid biosynthetic gene expression was confirmed using transgenic Arabidopsis seedlings expressing a dexamethasone (DEX)-inducible FUS3 and Arabidopsis mesophyll protoplasts transiently expressing the FUS3 gene. By accommodating the current evidence, we propose a hierarchical architecture of the transcriptional network in Arabidopsis seeds in which the oil biosynthetic pathway is integrated through the master transcriptional factor FUS3.

Co-localized intervals and candidate genes were identified for major and stable QTLs controlling pod weight and size on chromosomes A07 and A05 in an RIL population across four environments. Cultivated peanut (Arachis hypogaea L.) is an important legume crops grown in > 100 countries. Hundred-pod weight (HPW) is an important yield trait in peanut, but its underlying genetic mechanism was not well studied. In this study, a mapping population (Xuhua 13 × Zhonghua 6) with 187 recombinant inbred lines (RILs) was developed to map quantitative trait loci (QTLs) for HPW together with pod length (PL) and pod width (PW) by both unconditional and conditional QTL analyses. A genetic map covering 1756.48 cM was constructed with 817 markers. Additive effects, epistatic interactions, and genotype-by-environment interactions were analyzed using the phenotyping data generated across four environments. Twelve additive QTLs were identified on chromosomes A05, A07, and A08 by unconditional analysis, and five of them (qPLA07, qPLA05.1, qPWA07, qHPWA07.1, and qHPWA05.2) showed major and stable expressions in all environments. Conditional QTL mapping found that PL had stronger influences on HPW than PW. Notably, qHPWA07.1, qPLA07, and qPWA07 that explained 17.93-43.63% of the phenotypic variations of the three traits were co-localized in a 5 cM interval (1.48 Mb in physical map) on chromosome A07 with 147 candidate genes related to catalytic activity and metabolic process. In addition, qHPWA05.2 and qPLA05.1 were co-localized with minor QTL qPWA05.2 to a 1.3 cM genetic interval (280 kb in physical map) on chromosome A05 with 12 candidate genes. This study provides a comprehensive characterization of the genetic components controlling pod weight and size as well as candidate QTLs and genes for improving pod yield in future peanut breeding.