Mesenchymal stromal cells (MSCs) in bone marrow are important for bone homeostasis. Although platelet-derived growth factor (PDGF) has been reported to be involved in osteogenic differentiation of MSCs, the role remains controversial and the network of PDGF signaling for MSCs has not been clarified. To clarify the underlying regulatory mechanism of MSC functions mediated by PDGF, we deleted the PDGF receptor (PDGFR)␤ gene by Cre-loxP strategy and examined the role of PDGF in osteogenic differentiation of MSCs and fracture repair. In cultured MSCs, the mRNA expression of PDGF-A, -B, -C, and -D as well as PDGFR␣ and ␤ was detected. Depletion of PDGFR␤ in MSCs decreased the mitogenic and migratory responses and enhanced osteogenic differentiation as evaluated by increased alkaline phosphatase (ALP) activity and mRNA levels of ALP, osteocalcin (OCN), bone morphogenetic protein (BMP) 2, Runx2, and osterix in quantitative RT-PCR. PDGF-BB, but not PDGF-AA, inhibited osteogenic differentiation accompanied by decreased ALP activity and mRNA levels, except for BMP2. These effects of PDGF-BB were eliminated by depletion of PDGFR␤ in MSCs except that PDGF-BB still suppressed osterix expression in PDGFR␤-depleted MSCs. Depletion of PDGFR␤ significantly increased the ratio of woven bone to callus after fracture. From the combined analyses of PDGF stimulation and specific PDGFR␤ gene deletion, we showed that PDGFR␤ signaling distinctively induces proliferative and migratory responses but strongly inhibits osteogenic differentiation of MSCs. The effects of PDGFR␣ on the osteogenic differentiation were very subtle. PDGFR␤ could represent an important target for guided tissue regeneration or tissue engineering of bone.

It is demonstrated for the first time that mycoheterotrophy evolved after the establishment of mixotrophy rather than through direct shifts from autotrophy to mycoheterotrophy. This may be one of the principal patterns in the evolution of mycoheterotrophy. The results also suggest that the establishment of symbiosis with ectomycorrhizal fungi in the lineage leading to mixotrophic Cymbidium served as pre-adaptation to the evolution of the mycoheterotrophic species. Similar processes of nutritional innovations probably occurred in several independent orchid groups, allowing niche expansion and radiation in Orchidaceae, probably the largest plant family.

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The lionfish is an iconic marine fish, and recently renowned for a disastrous introduction into the West Atlantic. Genetic surveys of the putative invaders (Pterois volitans and Pterois miles) in their natural Indo-Pacific range can illuminate both topics. Previous research indicated that P. volitans and P. miles are sister species that hybridize in the invasive range, but hybridization in the native range is unknown. Here, we apply mtDNA COI and 2 nuclear introns (S7 RP1 and Gpd2) from 229 lionfish including the 2 invaders and 2 closely-related taxa (44 P. miles, 91 P. volitans, 31 Pterois lunulata, and 63 Pterois russelii) from 10 locations in their native ranges. Genetic data are supplemented with key morphological characters: dorsal, anal, and pectoral fin ray counts. We observed 2 lineages (d = 4.07%, 0.89%, and 2.75% at COI, S7 RP1, and Gpd2, respectively) among the 4 putative species: an Indian Ocean lineage represented by P. miles, and a Pacific Ocean lineage represented by P. lunulata and P. russelii. All specimens of the invasive P. volitans appear to be hybrids between the Indian Ocean P. miles and a Pacific lineage encompassing P. lunulata/russelii, a conclusion supported by both genetics and morphology. The divergences between Indian and Pacific forms are within the range of species-level partitions in fishes, and we recommend retention of the names P. miles and P. russelii for Indian and Pacific forms. The hybrid origin of the Atlantic invasion invokes the possibility of heterosis as a contributing factor to invasion success.

Intervertebral disc (IVD) degeneration is a major cause of low back pain. The transcription factor c-Fos/Activator Protein-1 (AP-1) controls the expression of inflammatory cytokines and matrix metalloproteinases (MMPs) that contribute to the pathogenesis IVD degeneration. We investigated the effects of inhibition of c-Fos/AP-1 on IVD degeneration and associated pain. A selective inhibitor, T-5224, significantly suppressed the interleukin-1β-induced up-regulation of Mmp-3, Mmp-13 and Adamts-5 transcription in human nucleus pulposus cells and in a mouse explant culture model of IVD degeneration. We used a tail disc percutaneous needle puncture method to further assess the effects of oral administration of T-5224 on IVD degeneration. Analysis of disc height, T2-magnetic resonance imaging (MRI) findings, and histology revealed that IVD degeneration was significantly mitigated by T-5224. Further, oral administration of T-5224 ameliorated pain as indicated by the extended tail-flick latency in response to heat stimulation of rats with needle-puncture-induced IVD degeneration. These findings suggest that the inhibition of c-Fos/AP-1 prevents disc degeneration and its associated pain and that T-5224 may serve as a drug for the prevention of IVD degeneration.