Anti-miR-10b

Hypertension is a multifactorial condition in which several genetic and environmental elements contribute. Recent investigations have revealed contribution of non-coding region of the transcriptome in this trait. CDKN2B-AS1, AK098656, MEG3, H19, PAXIP1-AS1, TUG1, GAS5, CASC2 and CPS1-IT are among long non-coding RNAs participating in the pathophysiology of hypertension. Several miRNAs have also been found to be implicated in this disorder. miR-296, miR-637, miR-296, miR-637, hsa-miR-361-5p, miR-122-5p, miR-199a-3p, miR-208a-3p, miR-423-5p, miR-223-5p and miR-140-5p are among dysregulated miRNAs in this condition whose application as diagnostic biomarkers for hypertension has been evaluated. Finally, hsa-circ-0005870, hsa_circ_0037911 and hsa_circ_0014243 are examples of dysregulated circular RNAs in hypertensive patients. In the current review, we describe the role of these non-coding RNAs in the pathophysiology of hypertension.

Pulmonary metastases pose treatment challenges for many cancers, including triple‐negative breast cancer (TNBC). A novel suicide gene and therapeutic microRNAs (miRs) combination therapy against lung metastases in vivo is tested in mouse models after intranasal delivery using nontoxic gold nanoparticles (AuNPs) formulated to carry these molecular therapeutics. AuNPs coated with chitosan‐β‐cyclodextrin (CS‐CD) are used and functionalized with a urokinase plasminogen activator (uPA) peptide to carry triple cancer suicide genes (thymidine kinase‐p53‐nitroreductase: TK‐p53‐NTR) plus therapeutic miRNAs (antimiR‐21, antimiR‐10b and miR‐100). Three AuNPs are synthesized: 20 nm gold nanodots (AuND), and 20 nm or 50 nm nanostars (AuNS), all surface coated with CS‐CD using a microfluidic‐optimized method. These positively charged AuNP‐CS‐CD cores are sequentially coated with synthetic miRNAs followed by TK‐p53‐NTR via electrostatic interactions, and uPA peptide is added through CD‐adamantane hostguest chemistry. Transfection efficiency comparisons for different AuNPs shows 50 nm AuNS allows ≈4.16‐fold higher gene transfection than other AuNPs. Intranasal delivery of uPA‐AuNS‐TK‐p53‐NTR‐microRNAs NPs (pAuNS@TK‐p53‐NTR‐miRs) in mice predominantly accumulates in lungs and facilitates ganciclovir and CB1954 prodrug‐mediated gene therapy against TNBC lung metastases. This new nanosystem can serve as an adaptable‐across‐cancer‐type, facile, and clinically scalable platform to allow future inhalational suicide gene‐miR combination therapy for patients harboring pulmonary metastases.