Class I TCP in fruit development: much more than growth.

Fruit development can be viewed as the succession of three main steps consisting of the fruit initiation, growth and ripening. These processes are orchestrated by different factors, notably the successful fertilization of flowers, the environmental conditions and the hormones whose action is coordinated by a large variety of transcription factors. Among the different transcription factor families, TEOSINTE BRANCHED 1, CYCLOIDEA, PROLIFERATING CELL FACTOR (TCP) family has received little attention in the frame of fruit biology despite its large effects on several developmental processes and its action as modulator of different hormonal pathways.

SlZHD17 is involved in the control of chlorophyll and carotenoid metabolism in tomato fruit.

Chlorophylls and carotenoids are essential and beneficial substances for both plant and human health. Identifying the regulatory network of these pigments is necessary for improving fruit quality. In a previous study, we identified an R2R3-MYB transcription factor, SlMYB72, that plays an important role in chlorophyll and carotenoid metabolism in tomato fruit.

BEL1-LIKE HOMEODOMAIN4 regulates chlorophyll accumulation, chloroplast development, and cell wall metabolism in tomato fruit.

Tomato (Solanum lycopersicum) is a model plant for studying fruit development and ripening. In this study, we found that down-regulation of a tomato bell-like homeodomain 4 (SlBL4) resulted in a slightly darker-green fruit phenotype and increased accumulation of starch, fructose, and glucose. Analysis of chlorophyll content and TEM observations was consistent with these phenotypes, indicating that SlBL4 was involved in chlorophyll accumulation and chloroplast formation.

Overexpression of the KNOX gene Tkn4 affects pollen development and confers sensitivity to gibberellin and auxin in tomato.

The knotted1-like homeobox genes not only regulate the formation and differentiation of meristems and vascular system but are also involved in biosynthesis and signal transduction of diverse plant hormones in tomato. Here, we showed that a knotted1-like homeobox gene Tkn4 is required for pollen and pollen tube growth when this gene is overexpressed in tomato. Pollen grains in the Tkn4 overexpressed plants (Tkn4-OX) germinated quicker than those in the wild-type (WT) plant cultured in vitro in germination media.

ATN-161 as an Integrin α5β1 Antagonist Depresses Ocular Neovascularization by Promoting New Vascular Endothelial Cell Apoptosis.

BACKGROUND ATN-161 (Ac-PHSCN-NH2), an antagonist of integrin α5β1, has shown an important influence in inhibiting tumor angiogenesis and metastasis of other tumor types. However, the mechanism of action of ATN-161 and whether it can inhibit ocular neovascularization (NV) are unclear. This study investigated the role of ATN-161 in regulating ocular angiogenesis in mouse models and explored the underlying signaling pathway.

Flt3 Regulation in the Mononuclear Phagocyte System Promotes Ocular Neovascularization.

Fms-like tyrosine kinase 3 (Flt3), a tyrosine kinase receptor expressed in CD34+ hematopoietic stem/progenitor cells, is important for both normal myeloid and lymphoid differentiation. It has been implicated in mice and humans for potential multilineage differentiation. We found that mice deficient in Flt3 or mice that received an Flt3 inhibitor (AC220) showed significantly reduced areas of ischemia-induced retinal neovascularization (RNV) and laser-induced choroidal NV (CNV) ( < 0.

Inhibition of integrin α5β1 ameliorates VEGF-induced retinal neovascularization and leakage by suppressing NLRP3 inflammasome signaling in a mouse model.

Purpose: To assess the effect of inhibiting integrin α5β1 by ATN-161 on vascular endothelial growth factor (VEGF)-induced neovascularization (NV) and leakage causing retinal detachment in adult Tet/opsin/VEGF transgenic mice, and characterize the underlying mechanism of its function.

Method: Retinas from adult Tet/opsin/VEGF transgenic mice and human retinal endothelial cells (HRECs) exposed to VEGF (treated with ATN-161 or PBS) were used to carry out immunofluorescence, RT-PCR and western blot to examine expression levels of integrin α5β1 and the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome. Retinal frozen section analysis was used to assess NV and leakage causing retinal detachment.

Endocan Blockade Suppresses Experimental Ocular Neovascularization in Mice.

Purpose: Ocular neovascularization (NV) is a pathologic process characterized by the proliferation and infiltration of various types of cells such as RPE, glial, and endothelial cells, which interact with proangiogenic factors and inflammatory cytokines. Endocan is known to be enriched in retinal endothelial tip cells under hypoxia, but the effect of endocan on ocular NV progression is largely unknown. In this study, we investigated the role of endocan in the ocular NV pathologic process and the possible mechanisms involved.

Identification of different macrophage subpopulations with distinct activities in a mouse model of oxygen-induced retinopathy.

The aim of the present study was to characterize the phenotypic shift, quantity and role changes in different subgroups of retinal macrophages in a mouse model of oxygen-induced retinopathy (OIR). The mRNA expression levels of macrophage M1 and M2 subgroup marker genes and polarization-associated genes were analyzed by RT-qPCR. The number of M1 and M2 macrophages in our mouse model of OIR was analyzed by flow cytometry at different time points during the progression of OIR.

Neutralization of IL-23 depresses experimental ocular neovascularization.

Interleukin-23 (IL-23) is a heterodimeric cytokine that consists of p19, a novel subunit, and p40, which is shared by IL-12. IL-23 has been demonstrated to play an important role in autoimmunity and tumor growth. However, the role of IL-23 in ocular neovascularization (NV) diseases remains unclear.

Interleukin-17A neutralization alleviated ocular neovascularization by promoting M2 and mitigating M1 macrophage polarization.

Neovascularization (NV), as a cardinal complication of several ocular diseases, has been intensively studied, and research has shown its close association with inflammation and immune cells. In the present study, the role of interleukin-17A (IL-17A) in angiogenesis in the process of ocular NV both in vivo and in vitro was investigated. Also, a paracrine role of IL-17A was demonstrated in the crosstalk between endothelial cells and macrophages in angiogenesis.

Pigment epithelium-derived factor regulates glutamine synthetase and l-glutamate/l-aspartate transporter in retinas with oxygen-induced retinopathy.

Purpose: A predominant function of Müller cells is to regulate glutamate levels, but these cells are compromised in oxygen-induced retinopathy. The aim of this study was to investigate the role of pigment epithelium-derived factor (PEDF) in regulating glutamate levels in retina under hypoxia.

Materials And Methods: One-week-old C57BL/6J mice were exposed to 75% oxygen for 5 days and then kept in room air for another 5 days to establish the oxygen-induced retinopathy (OIR) mouse model.

Improvement and optimization of standards for a preclinical animal test model of laser induced choroidal neovascularization.

Background: As the murine model of laser-induced choroidal neovascularization (CNV) is becoming the most established and commonly utilized model worldwide for studying the pathogenesis of CNV and its response to treatment, specific operating standards are yet to be clarified. The purpose of this study is to compare the lesion size of CNV in mice with different ages, sex, durations of CNV process, and treated positions of laser spots, to make recommendations that may improve and optimize the quality of the model.

Methods And Results: C57/BL6 mice of different ages were treated with diode laser photocoagulation per eye and perfused with PBS containing fluorescein-labeled dextran at different time of observation.