SPR setups and experimental procedures.

<p>(A) Schematic illustration of the SPR device: The He-Ne laser penetrated through a polarizer and a beam splitter, which split the beam 50/50. One was detected by a photodiode and the other one was coupled by a prism to generate Surface Plasmon Wave on the Au chip in which the angle shift was detected by a photodiode. (B) The OB-cadherin expressing cells flowing into the chamber were captured by the Au chip pre-coated with OB-cadherin antibodies, which changed the angle of the reflected laser beam. (C) A typical graphical data from SPR measurements.</p

Figure 3

<p>(A) Raman spectra of MSCs during osteogenic differentiation from 900 to 1800 cm⁻¹. (B) Magnified detail region for species from 900 to 1020 cm⁻¹ in stack diagram. OCP at 957 cm⁻¹ decreased upon osteogenic differentiation; β-TCP at 970 cm⁻¹ transiently appeared at Day 9 and HAP at 960 cm⁻¹ significantly increased after day9.</p

Figure 2

<p>(A) Background signal of Raman spectra. Magnified details of the region for control and cell species from 900 to 1020 cm⁻¹ in stack diagram.</p

Figure 5

<p>(A) Micrographs of MSCs treated with osteogenic media for 0, 3, 9, 15 and 24 days. (Scale bar: 100 µm) (B) Gene expression profiles of RUNX2, periostin, and type I collagen were detected in MSCs after Raman measurements by qPCR and normalized by internal and undifferentiated controls. Data are shown as mean ± SE (n = 3). (C) Alkaline phosphatase and Von Kossa staining of MSC-osteoblast differentiation. (D) Gene expression profiles of RUNX2, periostin, and type I collagen in staining samples were detected by qPCR and normalized by internal and undifferentiated controls. Data are shown as mean ± SE (n = 3).</p

MiR-155 targeting SHIP1 under hyperstretch.

<p>Stretch-reduction of SHIP1 is reversed by anti-miR-155 (A), but not pre-miR-155 (C), compared with non-specific control anti-miR and control pre-miR, respectively. Relative intensity of SHIP1 protein expression was normalized to the expression ofβ-actin and static control. (C) Determination of SHIP1 is a direct target for miR-155 by using SHIP1 3′-UTR luciferase activity with/without anti-miR-155 treatment under hyperstretch. The changes in luciferase activity are relative to static control. Data represent mean ± s.e.m. *, P<0.05; n = 5.</p

Schematic representation of the role of hyperstretch and hMSC in pulmonary cell inflammation.

<p>Hyperstretch induces miR-155 to target SHIP1, which leads to the increases of JNK activation and consequential IL-8 secretion. Co-culture of hMSCs exhibits the anti-inflammation effects to reverse the hyperstretch-induced hBEC inflammatory responses.</p

The miRs expression in cells under inflammatory challenages.

<p>(A) The expression of miR-155 in asthmatic and normal lung tissues of mice. (B) Examination of hyperstretch-regulated miRs, where miR-155 was significantly increased. (C) Hyperstretch regulation of miR-155 in hBECs with or without hMSCs co-culture. Expression levels of hBEC miR-155 in mono-culture (first four bars), and in co-culture (5^th and 6^th bar) after treatments with (D) IL-10 antibodies, and (E) IL-10 receptor [IL-10R] blocking antibodies. The results demonstrated that hMSCs and IL-10 had similar effects on up-regulation of hyperstretch-induction miR-155 expression in hBEC. The changes in secretion level are relative to static control. Data represent mean ± s.e.m. *, P<0.05; **, P<0.01 n = 5.</p

Legislative Documents

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