Collagen and Beyond: A Comprehensive Comparison of Human ECM Properties Derived from Various Tissue Sources for Regenerative Medicine Applications

Patrawalla, Nashaita Y.; Kajave, Nilabh S.; Albanna, Mohammad Z.; Kishore, Vipuil

doi:10.3390/jfb14070363

Cited by 3 publications

(1 citation statement)

References 53 publications

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“…The alterations in both stiffness and the degradation of ECM contribute to the promotion of a malignant cancer phenotype ( 36 ). Collagen is the most frequent ECM scaffolding protein within the stroma that is related to ECM stiffness enhancement and tumor malignancy ( 13 , 37 ). The collagen family is classified into different groups based on triple helix domain, length, and molecular weight ( 15 ) and includes fibril collagens; fibril-associated collagens; network-forming collagens; collagens VI, VII, XXVI, and XXVIII; membrane collagen; and multiplexins ( 38 ).…”

Section: Discussionmentioning

confidence: 99%

Construction and analysis of a reliable five-gene prognostic signature for colon adenocarcinoma associated with the wild-type allelic state of the COL6A6 gene

Liu,

Zhang,

Song

et al. 2024

Transl Cancer Res

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Background Tumors emerge by acquiring a number of mutations over time. The first mutation provides a selective growth advantage compared to adjacent epithelial cells, allowing the cell to create a clone that can outgrow the cells that surround it. Subsequent mutations determine the risk of the tumor progressing to metastatic cancer. Some secondary mutations may inhibit the aggressiveness of the tumor while still increasing the survival of the clone. Meaningful mutations in genes may provide a strong molecular foundation for developing novel therapeutic strategies for cancer. Methods The somatic mutation and prognosis in colon adenocarcinoma (COAD) were analyzed. The copy number variation (CNV) and differentially expressed genes (DEGs) between the collagen type VI alpha 6 chain ( COL6A6 ) mutation ( COL6A6 -MUT) and the COL6A6 wild-type ( COL6A6 -WT) subgroups were evaluated. The independent prognostic signatures based on COL6A6 -allelic state were determined to construct a Cox model. The biological characteristics and the immune microenvironment between the two risk groups were compared. Results COL6A6 was found to be highly mutated in COAD at a frequency of 9%. Patients with COL6A6 -MUT had a good overall survival (OS) compared to those with COL6A6 -WT, who had a different CNV pattern. Significant differences in gene expression were established for 593 genes between the COL6A6 -MUT and COL6A6 -WT samples. Among them, MUC16, ASNSP1, PRR18, PEG10 , and RPL26P8 were determined to be independent prognostic factors. The internally validated prognostic risk model, constructed using these five genes, demonstrated its value by revealing a significant difference in patient prognosis between the high-risk and low-risk groups. Specifically, patients in the high-risk group exhibited a considerably worse prognosis than did those in the low-risk group. The high-risk group had a significantly higher proportion of patients over 60 years of age and patients in stage III. Moreover, the tumor immune dysfunction and exclusion (TIDE) score and the expression of human leukocyte antigen (HLA) family genes were all higher in the high-risk group than that in the low-risk group. Conclusions The allelic state of COL6A6 and the five associated DEGs were identified as novel biomarkers for the diagnosis and prognosis of COAD and may be therapeutic targets in COAD.

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Section: Discussionmentioning

confidence: 99%

Construction and analysis of a reliable five-gene prognostic signature for colon adenocarcinoma associated with the wild-type allelic state of the COL6A6 gene

Liu,

Zhang,

Song

et al. 2024

Transl Cancer Res

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An innovative 4D printing approach for fabrication of anisotropic collagen scaffolds

Patrawalla,

Liebendorfer,

Kishore

2024

Biofabrication

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Collagen anisotropy is known to provide the essential topographical cues to guide tissue-specific cell function. Recent work has shown that extrusion-based printing using collagenous inks yield 3D scaffolds with high geometric precision and print fidelity. However, these scaffolds lack collagen anisotropy. In this study, extrusion-based 3D printing was combined with magnetic alignment approach in an innovative 4D printing scheme to generate 3D collagen scaffolds with high degree of collagen anisotropy. Specifically, the 4D printing process parameters – collagen (Col):xanthan gum (XG) ratio (Col:XG; 1:1, 4:1, 9:1 v/v), streptavidin-coated magnetic particle concentration (SMP; 0, 0.2, 0.4 mg/ml), and print flow speed (2, 3 mm/s) - were modulated and the effects of these parameters on rheological properties, print fidelity, and collagen alignment were assessed. Further, the effects of collagen anisotropy on human MSC (hMSC) morphology, orientation, metabolic activity, and ligamentous differentiation were investigated. Results showed that increasing the XG composition (Col:XG 1:1) enhanced ink viscosity and yielded scaffolds with good print fidelity but poor collagen alignment. On the other hand, use of inks with lower XG composition (Col:XG 4:1 and 9:1) together with 0.4 mg/ml SMP concentration yielded scaffolds with high degree of collagen alignment albeit with suboptimal print fidelity. Modulating the print flow speed conditions (2 mm/s) with 4:1 Col:XG inks and 0.4 mg/ml SMP resulted in improved print fidelity of the collagen scaffolds while retaining high level of collagen anisotropy. Cell studies revealed hMSCs orient uniformly on aligned collagen scaffolds. More importantly, collagen anisotropy was found to trigger tendon or ligament-like differentiation of hMSCs. Together, these results suggest that 4D printing is a viable strategy to generate anisotropic collagen scaffolds with significant potential for use in musculoskeletal tissue engineering applications.

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Cardiac tissue engineering: an emerging approach to the treatment of heart failure

Rayat Pisheh,

Nojabaei,

Darvishi

et al. 2024

Front. Bioeng. Biotechnol.

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Heart failure is a major health problem in which the heart is unable to pump enough blood to meet the body’s needs. It is a progressive disease that becomes more severe over time and can be caused by a variety of factors, including heart attack, cardiomyopathy and heart valve disease. There are various methods to cure this disease, which has many complications and risks. The advancement of knowledge and technology has proposed new methods for many diseases. One of the promising new treatments for heart failure is tissue engineering. Tissue engineering is a field of research that aims to create living tissues and organs to replace damaged or diseased tissue. The goal of tissue engineering in heart failure is to improve cardiac function and reduce the need for heart transplantation. This can be done using the three important principles of cells, biomaterials and signals to improve function or replace heart tissue. The techniques for using cells and biomaterials such as electrospinning, hydrogel synthesis, decellularization, etc. are diverse. Treating heart failure through tissue engineering is still under development and research, but it is hoped that there will be no transplants or invasive surgeries in the near future. In this study, based on the most important research in recent years, we will examine the power of tissue engineering in the treatment of heart failure.

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Collagen and Beyond: A Comprehensive Comparison of Human ECM Properties Derived from Various Tissue Sources for Regenerative Medicine Applications

Cited by 3 publications

References 53 publications

Construction and analysis of a reliable five-gene prognostic signature for colon adenocarcinoma associated with the wild-type allelic state of the COL6A6 gene

Construction and analysis of a reliable five-gene prognostic signature for colon adenocarcinoma associated with the wild-type allelic state of the COL6A6 gene

An innovative 4D printing approach for fabrication of anisotropic collagen scaffolds

Cardiac tissue engineering: an emerging approach to the treatment of heart failure

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