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Cross Bridges of GB Smooth Muscle Contraction
Published in Wenguang Li, Biliary Tract and Gallbladder Biomechanical Modelling with Physiological and Clinical Elements, 2021
Additional experiments (Yu et al. 1993, 1994, 1998) showed that CCK initially bound to Giα3 (a G protein) in the cell membrane. In response to activation of G-protein-coupled receptors, the phosphatidylinositol-specific phospholipase C beta 3 (PLC-β3) hydrolyses phosphatidylinositol biphosphate (PIP2) into inositol 1,4,5-triphosphate (IP3) and diacylglycerol (DAG). At a high dose of CCK, IP3 stimulates sarcoplasmic reticulum (SR) to release more Ca2+, which then binds to calmodulin (CaM), activating myosin light-chain kinase (MLCK) to allow myosin to be phosphorylated (P-myosin). In this case, CaM inhibits the protein kinase C (PKC) pathway (Harnett et al. 2005). The P-myosin attaches to actin filaments and creates cross bridges to generate tension (Yu et al. 1998). The CCK activation pathway is illustrated in Figure 7.1.
Imaging Angiogenesis
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
More recently, a technetium-99m-labeled SPECT tracer (99mTc-NC100692, maraciclatide) was introduced for the imaging of αvβ3 integrin expression in various preclinical animal models of tumor- and ischemia-induced angiogenesis. This tracer, characterized by a very high affinity (∼1 nM) and renal clearance route, was demonstrated to successfully evaluate αvβ3 integrin expression in subcutaneous and orthotopic tumors (Dearling et al. 2013), peripheral angiogenesis in murine model of hindlimb ischemia (Hua et al. 2005; Dobrucki et al. 2009), and myocardial angiogenesis in mice lacking the MMP-9 gene (Lindsey et al. 2006) and in rats subjected to the local adenoviral delivery of the insulin-like growth factor-1 (IGF-1) injected into the peri-infarct region (Figure 30.1) (Dobrucki et al. 2010b).
Polymeric Hydrogels via Click Chemistry for Regenerative Engineering
Published in Yusuf Khan, Cato T. Laurencin, Regenerative Engineering, 2018
Liangju Kuang, Paul A. Lengemann, Meng Deng
Generally, a gelation time of several hours or days at room temperature is necessary for DA-formed hydrogels. To overcome this obstacle of the DA-formed hydrogels, Yu et al. prepared a novel biological hydrogel from HA and PEG using DA click chemistry. By simply tuning the furyl-to-maleimide molar ratio and the substitution degree of the furyl group, the value of the compressive modulus was controlled from 4.86 ± 0.42 to 75.90 ± 5.43 kPa, and the gelation time could be tuned from 412 to 51 minutes at 37°C. Moreover, the DA-formed hydrogel was utilized to investigate the cell encapsulation viability and the influence of gelation time on encapsulated cell survival. The results showed that a gelation time of about 1 hour was suitable for cell viability, proliferation, and chondrogenesis. The gene expression levels of the chondrogenesis markers collagen II and aggrecan were significantly upregulated both with and without growth factor TGF-β3. Additionally, as shown in Figure 2.3, the HA/PEG hydrogel showed outstanding load-bearing and shape recovery properties even after 2,000 loading cycles, mimicking the mechanical properties and behavior of articular cartilage [28].
Heparin mimics and fibroblast growth factor-2 fabricated nanogold composite in promoting neural differentiation of mouse embryonic stem cells
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Fei Yu, Shaoyu Cheng, Jiehua Lei, Yingjie Hang, Qi Liu, Hongwei Wang, Lin Yuan
Further studies on the transcript levels of β3-tubulin, the marker gene for mature nerve cells, showed the similar results to Nestin’s expression. AuNP/FGF2, AuNP-PMS and PMS/FGF2 can all promote the expression of β3-tubulin, about 1.4, 5.7 and 9.2 times higher than that of the blank, respectively (Figure 5B). As expected, the induction effect of AuNP-PMS/FGF2 nanoparticle composite on β3-tubulin expression is the strongest in all treatments, about 15 times as high as that of blank. The results from β3-tubulin mRNA expression indicated that AuNP-PMS/FGF2 nanoparticle composite could effectively promote the transition of mouse stem cells into mature neuron-like cells.
Critical-Size Alveolar Defect Treatment via TGF-ß3 and BMP-2 Releasing Hybrid Constructs
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Aybüke Garipcan, Petek Korkusuz, Elif Bilgic, Halil M. Aydin, Eda Ozturk, Ilyas Inci, Asya Ozkizilcik, K. Kamile Ozturk, Erhan Piskin, Ibrahim Vargel
After implantation, all of the osteogenic gene expressions on day 21 were significantly upregulated in S-GF-B-T group in comparison to control group indicating the presence of osteogenic differentiation and activity (Fig 3). In particular, ALP, OC, RUNX2 mRNA levels were slightly elevated in S-GF-B-T group relative to that of autograft group. Upregulation of those genes was mounting evidence for the active osteoblasts and bone formation in S-GF-B-T group whereas lower expression of those genes in the autograft group might be due to already existing bone graft in the defected area. BSP expression was upregulated in the autograft and the S-GF-B-T groups compared to control group. Also, increase in the expression levels of ON was observed in the autograft and S-GF-B-T groups. It could be expected to observe higher expression of BSP and ON in autograft group than that of the S-GF-B-T group, as autograft group represents the gold standard. However, the expression of BSP and ON indicates initial bone formation and osteoblast differentiation [63, 64, 65]. As explained above, the gene expression of osteogenesis markers was lower in autograft group possibly due to the presence of implanted bone graft. On the other hand, the upregulation in the expressions of BSP and ON genes, in S-GF-B-T group on day 21, may be caused by the differentiation signals from microenvironment or by slight BMP2 release in the first month which both can stimulate differentiation of osteoprogenitor cells recruited by TGF-β3 release. On the other hand, we could not observe upregulation in osteoblastic gene expressions in S-GF-B group similar to S-GF group. This result provided evidence that BMP-2 were not released at the first month, considerably and could not stimulate osteogenic differentiation alone as observed in S-GF-B-T. Regarding to gene expression results reported by Vural et al [23] commercial gelatin sponge containing BMP-2 encoding MSCs were upregulated RUNX2, ALP, OC gene expressions more than 2-fold. Here, for the dual combinations of TGF-β3, and BMP-2, we recorded 2.2, 8.6, 18.4-fold increase in RUNX2, ALP, OC gene expressions, respectively. These results showed that TGF-β3 alone seemed to be able to trigger osteogenesis in early time points. This result was also in correlation with the literature reporting the potential of TGF-β family members to initiate bone formation by recruiting osteoprogenitors to defect area [66, 67].