Table 1.
Pathways Downregulated in lr-MSC | Ref. No. | Pathways Upregulated in lr-MSC | Ref. No. |
---|---|---|---|
YAP1 (TAZ)-stimulated gene expression | 121, 125 | RUNX3 regulates WNT signaling | 121, 125 |
Interferon-γ signaling | 121, 125 | Elastic fiber formation | 121, 125 |
MPS IIID–Sanpilippo syndrome D | 121, 125 | Nuclear signaling by ERBB4 | 121, 125 |
Antagonism of activin by follstatin | 121, 125 | MET promotes cell motility | 121, 125 |
Gene and protein expression by JAK-STAT signaling after IL-12 stimulation | 121, 125 | MET activates PTPN11 | 121, 125 |
Interferon signaling | 121, 125 | MET activates STAT3 | 121, 125 |
IL-12 signaling | 121, 125 | Degradation of extracellular matrix | 121, 125 |
IL-12 family signaling | 121, 125 | MET activates PTK2 signaling | 121, 125 |
Glycoprotein hormones | 121, 125 | MET receptor activation | 121, 125 |
Regulation of active cofactor, UDP-glucuronate | 121, 125 | MET activates PI3K/AKT signaling | 121, 125 |
Peptide hormone biosynthesis | 121, 125 | Potassium transport channels | 121, 125 |
Transcriptional regulation by RUNX3 | 121, 125 | MET interacts with TNS proteins | 121, 125 |
Signaling by activin | 125 | MET activates PTPN11 | 121, 125, 148 |
Peptide hormone metabolism | 121, 125, 148 | MET activates STAT3 | 121, 125, 148 |
Regulation of PTEN localization | 121, 125, 148 | Regulation of IGF transport and uptake by insulin-like growth factor-binding proteins | 121, 125, 148 |
Cell proliferation | 124 | Posttranslational protein phosphorylation | 121, 125, 148 |
Cell growth | 124 | Extracellular matrix organization | 121, 125, 148 |
Response to wound healing | 124 | IL-4 and IL-13 signaling | 121, 125, 148 |
Oxidation-reduction processes | 124 | Laminin interactions | 121, 125, 148 |
Positive regulation of gene expression | 124 | Chemokine receptors bind chemokines | 121, 125, 148 |
Activation of GABAB receptors | 121, 125, 148 | ||
Degradation of extracellular matrix | 121, 125, 148 | ||
Nonintegrin membrane-ECM interactions | 121, 125, 148 | ||
GABA receptor activation | 121, 125, 148 | ||
Formation of β-catenin: TCF transactivating complex | 121, 125, 148 | ||
Platelet degranulation | 121, 125, 148 | ||
Response to elevated platelet cytosolic Ca2+ | 121, 125, 148 | ||
ECM proteoglycans | 121, 125, 148 | ||
Activation of G protein-gated potassium channels | 121, 125, 148 | ||
G protein-gated potassium channels | 121, 125, 148 | ||
Inhibition of voltage-gated Ca2+ channels via Gβ/γ-subunits | 121, 125, 148 | ||
Platelet activation, signaling, and aggregation | 121, 125, 148 | ||
Neurodegenerative diseases | 121, 125, 148 | ||
Deregulated CDK5 triggers multiple degenerative pathways in Alzheimer’s | 121, 125, 148 | ||
Myogenesis | 121, 125, 148 | ||
Inwardly rectifying K+ channels | 121, 125, 148 | ||
Oxidation-reduction process | 124 | ||
Cell proliferation | 124 | ||
Response to drug | 124 | ||
RNA splicing | 124 | ||
Protein folding | 124 | ||
Positive regulation of IκB/NF-κB signaling | 124 | ||
Metabolic process | 124 | ||
Reg mRNA stability | 124 |
Table comprises significantly different pathways between lung-resident mesenchymal stromal cells (lr-MSC) and bone marrow-derived mesenchymal stromal cells (BM-MSC), downregulated in lr-MSC compared with BM-MSC (left column) and upregulated in lr-MSC compared with BM-MSC (right column), determined by proteomic analysis. If enrichment analyses were not provided, we conducted our own analyses of the differentially expressed proteins, with P ≤ 0.05. These analyses were conducted using Reactome (https://reactome.org) using a cutoff of P ≤ 0.05 and are listed in italics above. YAP1, yes-associated protein 1; MPS IIID, mucopolysaccharidosis type IIID; JAK, Janus kinase; STAT, signal transducer and activator of transcription; IL, interleukin; PTEN, phosphatase and tensin homolog; RUNX3, runt-related transcription factor 3; WNT, wingless and Int-1; ERBB4, Erb-B2 receptor tyrosine kinase 4; MET, MET proto-oncogene, receptor tyrosine kinase; PTPN11, protein tyrosine phosphatase nonreceptor type 11; PTK2, protein tyrosine kinase 2; PI3K, phosphatidylinositol 3-kinase; AKT, protein kinase B; TNS, tensin proteins; IGF, insulin-like growth factor; GABAB, γ-aminobutyric acid B receptors; ECM, extracellular matrix; GABAA, γ-aminobutyric acid A receptors; TCF, T cell factor; CDK5, cyclin-dependent kinase 5; IκB, inhibitor of κB; NF-κB, nuclear factor-κB.