That is not the headline to the original study:
https://pubmed.ncbi.nlm.nih.gov/34807265/
This is the headline:
“The SARS-CoV-2 Spike protein disrupts human cardiac pericytes function through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease”
Did somebody miss the words “The SARS-CoV-2 Spike Protein?” This refers to the Spike Protein on the SARS-CoV-2 virus.
The Spike Protein is not in the mRNA vaccine. The vaccine only has the RNA molecule blueprint that the ribosomes use to translate into proteins (antigens) which are the broken up into fragments or taken up by helper T cells by MHC class II proteins. The process is a closed system. Where are there any Spike Proteins unleashed into the body?
Because the mRNA injected gets into cells and uses the cells machinery to produce the spike protein “signature” which is then identified by the body as a threat and generates antibodies to defend against it.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a broad range of clinical responses including prominent microvascular damage.What are pericytes?
The capacity of SARS-CoV-2 to infect vascular cells is still debated.
Additionally, the SARS-CoV-2 Spike (S) protein may act as a ligand to induce non-infective cellular stress.
We tested this hypothesis in pericytes (PCs), which are reportedly reduced in the heart of patients with severe coronavirus disease-2019 (COVID-19).
Here we newly show that the in vitro exposure of primary human cardiac PCs [pericytes] to the SARS-CoV-2 wildtype strain or the α [alpha] and δ [Delta] variants caused rare infection events.
Exposure to the recombinant S protein alone elicited signalling and functional alterations, including:
(1) increased migration,
(2) reduced ability to support endothelial cell (EC) network formation on Matrigel ["Matrigel resembles the laminin/collagen IV-rich basement membrane extracellular environment found in many tissues and is used by cell biologists as a substrate (basement membrane matrix) for culturing cells" - Wikipedia],
(3) secretion of pro-inflammatory molecules typically involved in the cytokine storm, and
(4) production of pro-apoptotic factors [mostly proteins having a role in apoptosis] causing EC [endothelial cell] death. Next, adopting a blocking strategy against the S protein receptors angiotensin-converting enzyme 2 (ACE2) and CD147, we discovered that the S protein stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) through the CD147 receptor, but not ACE2, in PCs [pericytes].
The neutralisation of CD147, either using a blocking antibody or mRNA silencing, reduced ERK1/2 activation, and rescued PC [pericyte] function in the presence of the S protein.
Immunoreactive S protein was detected in the peripheral blood of infected patients.
In conclusion, our findings suggest that the S protein may prompt PC [pericyte] dysfunction, potentially contributing to microvascular injury.
This mechanism may have clinical and therapeutic implications.
Pericytes are cells present at intervals along the walls of capillaries (and post-capillary venules).What is CD147?
In the CNS, they are important for blood vessel formation, maintenance of the blood–brain barrier, regulation of immune cell entry to the central nervous system (CNS) and control of brain blood flow.
Classically, the blood flow increase evoked by neuronal activity, which focuses the oxygen and glucose supply on active neurons and generates BOLD functional imaging signals, was thought to reflect relaxation of smooth muscle cells around arterioles.
Recently, however, it has become clear that much of the flow increase is generated by dilation of capillaries, rather than of arterioles (which dilate more slowly), and that this is achieved by a relaxation of contractile pericytes.
Pericytes also play a key role in pathology: in ischaemia [restriction of blood supply,] pericytes constrict capillaries, trapping blood cells, which prevents microcirculatory reperfusion [restoration of blood flow] after clot removal in stroke.
This has made pericytes an important therapeutic target.
In late 2019, the betacoronavirus SARS-CoV-2 was identified as the viral agent responsible for the coronavirus disease 2019 (COVID-19) pandemic.
Coronaviruses Spike proteins are responsible for their ability to interact with host membrane receptors and different proteins have been identified as SARS-CoV-2 interactors, among which Angiotensin-converting enzyme 2 (ACE2), and Basigin2/EMMPRIN/CD147 (CD147).
CD147 plays an important role in human immunodeficiency virus type 1, hepatitis C virus, hepatitis B virus, Kaposi's sarcoma-associated herpesvirus, and severe acute respiratory syndrome [SARS] coronavirus infections.
In particular, SARS-CoV recognizes the CD147 receptor expressed on the surface of host cells by its nucleocapsid protein binding to cyclophilin A (CyPA), a ligand for CD147.
However, the involvement of CD147 in SARS-CoV-2 infection is still debated.
Interference with both the function (blocking antibody) and the expression (knock down) of CD147 showed that this receptor partakes in SARS-CoV-2 infection and provided additional clues on the underlying mechanism:CD147 binding to CyPA does not play a role;Altogether, these findings suggest that CD147 is involved in SARS-CoV-2 tropism and represents a possible therapeutic target to challenge COVID-19. ["tropism refers to the way in which different viruses/pathogens have evolved to preferentially target specific host species, specific tissue, or specific cell types within those species" - Wikipedia]
CD147 regulates ACE2 levels and both receptors are affected by virus infection.