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"Gu Qi"
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Vascularized organ bioprinting: From strategy to paradigm
Over the past two decades, 3D bioprinting has become a popular research topic worldwide, as it is the most promising approach for manufacturing vascularized organs in vitro. However, transitioning from bioprinting of simple tissue models to real biomedical applications is still a challenge due to incomplete interdisciplinary theoretical knowledge and imperfect multi‐technology integration. This review examines the goals of vasculature manufacturing and proposes new strategic objectives in three stages. We then outline a bidirectional manufacturing strategy consisting of top‐down reconstruction (bioprinting) and bottom‐up regeneration (cellular behaviour). We also provide an in‐depth analysis of the four aspects of design, ink, printing and culture. Furthermore, we present the ‘construction‐comprehension cycle’ research paradigm and the ‘math‐model‐based batch insights generator’ research paradigm for the future, which may have the potential to revolutionize the biomedical field. This review examines the goals of vasculature manufacturing and suggests the objectives in three stages. Then, we outline a bidirectional manufacturing strategy through top‐down reproduction (bioprinting) and bottom‐up regeneration (cellular behaviour). Next, we introduce the views in detail from four links: design, ink, printing and culture. Furthermore, we present the ‘constructing‐comprehension cycle’ research paradigm in Strategic Priority Research Program (SPRP) and the ‘math‐model‐based batch insights generator’ research paradigm for the future with the potential to revolutionize the biomedical field. This review summarizes and distils the research results and ideas of the SPRP in the field of in vitro organ reconstruction and manufacturing. Unlike the common reviews in this field, this paper presents fresh ideas, highlights overlooked issues, corrects some misconceptions and points out future research directions.
Journal Article
Mitochondrial genome transfer drives metabolic reprogramming in adjacent colonic epithelial cells promoting TGFβ1-mediated tumor progression
Although nontumor components play an essential role in colon cancer (CC) progression, the intercellular communication between CC cells and adjacent colonic epithelial cells (CECs) remains poorly understood. Here, we show that intact mitochondrial genome (mitochondrial DNA, mtDNA) is enriched in serum extracellular vesicles (EVs) from CC patients and positively correlated with tumor stage. Intriguingly, circular mtDNA transferred via tumor cell-derived EVs (EV-mtDNA) enhances mitochondrial respiration and reactive oxygen species (ROS) production in CECs. Moreover, the EV-mtDNA increases TGFβ1 expression in CECs, which in turn promotes tumor progression. Mechanistically, the intercellular mtDNA transfer activates the mitochondrial respiratory chain to induce the ROS-driven RelA nuclear translocation in CECs, thereby transcriptionally regulating TGFβ1 expression and promoting tumor progression via the TGFβ/Smad pathway. Hence, this study highlights EV-mtDNA as a major driver of paracrine metabolic crosstalk between CC cells and adjacent CECs, possibly identifying it as a potential biomarker and therapeutic target for CC.
The interaction between colon cancer cells and colonic epithelial cells (CECs) is critical yet not well-known. Here, the authors show that tumor extracellular vesicles mediate mitochondrial DNA transfer to CECs, initiating mitochondrial activation and RelA-induced TGFβ1 expression, leading to tumor progression.
Journal Article
Characterisation of strength and deformation characteristics of alkali-activated rice husk ash filler-assemblage perimeter rock
In this study, the strength characteristics, deformation characteristics and damage characteristics of three kinds of specimens, namely, surrounding rock, cemented paste backfill (CPB) and a surrounding rock-CPB combination, were studied by uniaxial compression testing using rice husk ash and slag as cementing materials, and the mechanical properties of the combination specimens with different height ratios were also analyzed. The results showed that the surrounding rock specimens were the strongest, followed by the composite body, and the CPB was the weakest. The relationship between different height ratios of the assemblage and the cut line modulus was found according to the fitted curves. The CPB specimens and the surrounding rock specimens showed ductile damage, while the assemblage specimens showed brittle damage.
Journal Article
EphA1 Activation Induces Neuropathological Changes in a Mouse Model of Parkinson’s Disease Through the CXCL12/CXCR4 Signaling Pathway
There is increasing evidence that EphA1 is involved in the function and development of the central nervous system, especially in neuroinflammation. It has been found to affect the disease progression of Alzheimer’s disease (AD) by regulating the neuroinflammatory process. Neuroinflammation has always been regarded as the mechanism of the development of Parkinson’s disease (PD) and possible therapeutic targets. Therefore, it is worth studying whether EphA1 has a potential therapeutic value for PD. The purpose of this study is to investigate the effect of EphA1 in mice and PD cell models and its mechanism.
In this study, we verified the difference in expression of EphA1 and the effect and mechanism of EphA1 on neuropathological changes through Parkinson’s patient samples, Parkinson’s mice model, and Parkinson’s model prepared from SH-SY5Y cells in vitro.
EphA1 was highly expressed in the substantia nigra (SN) region of Parkinson mice and the Parkinson cell model, while the expression of tyrosine hydroxylase (TH) in the SN region of Parkinson mice was significantly reduced. After silenced EphA1 in the SH-SY5Y cell PD model, the expression levels of α-synuclein, inflammatory factors, and microglia-activated chemokine decreased. The co-immunoprecipitation experiment proved that EphA1 overexpression could promote the binding of CXCL12 and CXCR4. However, after silenced EphA1 and CXCL12 at the same time, the above effects brought by silenced EphA1 were suppressed. The same result appeared in mice with PD.
EphA1 improves the inflammatory responses and neuropathological changes of the PD model in vivo and in vitro through the CXCL12/CXCR4 signaling pathway.
Graphical abstract
Journal Article
3D biomimetic niche modulates embryo development in vitro
Embryo development undergoes critical morphological transformations post-implantation, largely driven by the complex and dynamic microenvironment of the uterus. Despite advances, current 3D culture models inadequately recapitulate the uterine environment necessary for studying embryo-uterus interactions. In this work, we engineer a hydrogel inspired by the properties of the decidua, incorporating Matrigel to support blastocyst implantation and embryo development in vitro. Our findings reveal that embryos cultured within this hydrogel system successfully progress to an early organogenesis-like stage, including the development of first and second heart fields, mimicking natural embryogenesis. Moreover, we identify that the mechanical properties, particularly stress relaxation, play a crucial role in facilitating focal adhesion (FA) formation between the trophoblast and the hydrogel. Additionally, the degradation of the hydrogel by embryo-secreted metalloproteinases (
MMP2
and
MMP9
) creates a favorable environment for continued embryonic growth and development. These insights contribute to a deeper understanding of how the external environment regulates embryo development and offer an enhanced approach for in vitro embryo culture.
The complex interactions between the uterus microenvironment and the embryo during development are not fully understood. Here, authors engineer a 3D hydrogel culture system to investigate how the physical and biochemical properties of the uterine microenvironment impact embryo development in vitro.
Journal Article
Proportion and clinical characteristics of metabolic-associated fatty liver disease and associated liver fibrosis in an urban Chinese population
Abstract
Background:
Metabolic-associated fatty liver disease (MAFLD) is the predominant form of chronic liver disease worldwide. This study was designed to investigate the proportion and characteristics of MAFLD within the general Chinese population and to identify the contributory risk factors for liver fibrosis among MAFLD individuals.
Methods:
The participants were recruited from a cohort undergoing routine health evaluations at the Third Hospital of Hebei Medical University between May 2019 and March 2023. The diagnosis of MAFLD was based on the established clinical practice guidelines. The fibrosis-4 index score (FIB-4) was employed to evaluate hepatic fibrosis, with a FIB-4 score of ≥1.3 indicating significant fibrosis. Binary logistic regression analyses were used to determine risk factors associated with significant hepatic fibrosis in MAFLD.
Results:
A total of 22,970 participants who underwent comprehensive medical examinations were included in the analysis. The overall proportion of MAFLD was 28.77% (6608/22,970), with 16.87% (1115/6608) of these patients showing significant fibrosis as assessed using FIB-4. Independent risk factors for significant liver fibrosis in MAFLD patients were male (odds ratio [OR] = 0.676, 95% confidence interval [CI]: 0.558–0.821), hepatitis B surface antigen (HBsAg) positivity (OR = 2.611, 95% CI: 1.557–4.379), body mass index ≥23.00 kg/m2 (OR = 0.632, 95% CI: 0.470–0.851), blood pressure ≥130/85 mmHg (OR = 1.885, 95% CI: 1.564–2.272), and plasma glucose ≥5.6 mmol/L (OR = 1.815, 95% CI: 1.507–2.186) (all P <0.001).
Conclusions:
The proportion of MAFLD in an urban Chinese population is 28.77%. About 16.87% of MAFLD patients presented with significant liver fibrosis. Independent risk factors for significant liver fibrosis in MAFLD patients should be noticed.
Journal Article
Parasitic insect-derived miRNAs modulate host development
Parasitic wasps produce several factors including venom, polydnaviruses (PDVs) and specialized wasp cells named teratocytes that benefit the survival of offspring by altering the physiology of hosts. However, the underlying molecular mechanisms for the alterations remain unclear. Here we find that the teratocytes of
Cotesia vestalis
, an endoparasitoid of the diamondback moth
Plutella xylostella
, and its associated bracovirus (CvBV) can produce miRNAs and deliver the products into the host via different ways. Certain miRNAs in the parasitized host are mainly produced by teratocytes, while the expression level of miRNAs encoded by CvBV can be 100-fold greater in parasitized hosts than non-parasitized ones. We further show that one teratocyte-produced miRNA (Cve-miR-281-3p) and one CvBV-produced miRNA (Cve-miR-novel22-5p-1) arrest host growth by modulating expression of the host ecdysone receptor (
EcR
). Altogether, our results show the first evidence of cross-species regulation by miRNAs in animal parasitism and their possible function in the alteration of host physiology during parasitism.
The moth
Plutella xylostella
during its larval stage is the host of the endoparasitic wasp
Cotesia vestalis
. Here the authors show that the parasitoids deliver microRNAs to their hosts through their symbiotic virus and specialized cells leading to induced developmental delay.
Journal Article